il 10  (Boster Bio)


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    Structured Review

    Boster Bio il 10
    P-A regulates expression of IL-6, <t>IL-10,</t> and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Il 10, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 38 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    2) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    3) Product Images from "Deep rTMS Mitigates Behavioral and Neuropathologic Anomalies in Cuprizone-Exposed Mice Through Reducing Microglial Proinflammatory Cytokines"

    Article Title: Deep rTMS Mitigates Behavioral and Neuropathologic Anomalies in Cuprizone-Exposed Mice Through Reducing Microglial Proinflammatory Cytokines

    Journal: Frontiers in Integrative Neuroscience

    doi: 10.3389/fnint.2020.556839

    rTMS alleviates the CPZ-induced changes in expression levels of inflammatory cytokines in CPU, FC, and HIP of mice. (A) The bar chart shows the statistical analytic results of IL-1β levels in the three brain regions of the mice. (B) The bar chart shows the statistical analytic results of IL-6 levels in the three brain regions of the mice. (C) The bar chart shows the statistical analytic results of IL-10 levels in the three brain regions of the mice. Data are expressed as mean ± SD. N = 7/group. * p
    Figure Legend Snippet: rTMS alleviates the CPZ-induced changes in expression levels of inflammatory cytokines in CPU, FC, and HIP of mice. (A) The bar chart shows the statistical analytic results of IL-1β levels in the three brain regions of the mice. (B) The bar chart shows the statistical analytic results of IL-6 levels in the three brain regions of the mice. (C) The bar chart shows the statistical analytic results of IL-10 levels in the three brain regions of the mice. Data are expressed as mean ± SD. N = 7/group. * p

    Techniques Used: Expressing, Mouse Assay

    4) Product Images from "Butyrate as a bioactive human milk protective component against food allergy, et al. Butyrate as a bioactive human milk protective component against food allergy"

    Article Title: Butyrate as a bioactive human milk protective component against food allergy, et al. Butyrate as a bioactive human milk protective component against food allergy

    Journal: Allergy

    doi: 10.1111/all.14625

    Preventive HM butyrate action against FA in the animal model. A, The experimental design of the food allergy mouse model. Four‐week‐old female C3H/HeJ mice (n = 4 in each group) were used in the FA animal model. Two weeks before first sensitization, oral gavage with 30 mg/kg/d of butyrate was started and continued throughout the study. The mice were sensitized orally on days 0, 7, 14, 21, and 28, with 20 mg of BLG, 1 mg of OVA, or 12 mg of PN mixed with 10 μg cholera toxin (CT) as adjuvant. The control mice receive CT only. On day 35, the mice were challenged by gavage with BLG (50 mg), OVA (5 mg), or PN (36 mg). Anaphylaxis scores and rectal temperatures were assessed for 1 h after challenge, and blood samples were collected to measure mMCP‐1 and sIgE. After 24 h, the mice were killed, and their serum and tissues were collected. Two independent experiments were performed. Oral butyrate treatment significantly reduced anaphylactic score (B), serum MCP‐1 (C) and sIgE levels against BLG (D), OVA (E), and PN (F). Splenocytes from FA‐sensitized mice were stimulated 1 μg/mL of anti‐CD3 (clone 2C11) or 200 μg/mL BLG/OVA/PN and incubated at 37°C for 72 h. Butyrate inhibited IL‐4 (G) and IL‐13 (H) production and stimulated IL‐10 (I) and IFN‐γ (L) production in BLG‐, OVA‐, and PN‐sensitized mice. H 2 O 2 yield (M), SOD (N), and ROS‐induced damage on aconitase activity (O) were measured in hepatic mitochondria. The mitochondrial ROS‐induced dysfunction was proven by the higher mitochondrial H 2 O 2 yield, higher SOD activity, and lower basal/total aconitase ratio observed in all FA‐sensitized animals compared with the control group. Butyrate administration positively modulates the oxidative stress as demonstrated by the lower H 2 O 2 release, the decreased SOD activity, and the reactivation of the aconitase enzyme in all treated groups compared with control animals. Data are representative of at least 2 independent experiments, reported as median with range, and analyzed using the unpaired t test. BLG, mice sensitized with β‐lactoglobulin; CTRL, control mice; OVA, mice sensitized with ovalbumin; PN, mice sensitized with peanut extract. * P
    Figure Legend Snippet: Preventive HM butyrate action against FA in the animal model. A, The experimental design of the food allergy mouse model. Four‐week‐old female C3H/HeJ mice (n = 4 in each group) were used in the FA animal model. Two weeks before first sensitization, oral gavage with 30 mg/kg/d of butyrate was started and continued throughout the study. The mice were sensitized orally on days 0, 7, 14, 21, and 28, with 20 mg of BLG, 1 mg of OVA, or 12 mg of PN mixed with 10 μg cholera toxin (CT) as adjuvant. The control mice receive CT only. On day 35, the mice were challenged by gavage with BLG (50 mg), OVA (5 mg), or PN (36 mg). Anaphylaxis scores and rectal temperatures were assessed for 1 h after challenge, and blood samples were collected to measure mMCP‐1 and sIgE. After 24 h, the mice were killed, and their serum and tissues were collected. Two independent experiments were performed. Oral butyrate treatment significantly reduced anaphylactic score (B), serum MCP‐1 (C) and sIgE levels against BLG (D), OVA (E), and PN (F). Splenocytes from FA‐sensitized mice were stimulated 1 μg/mL of anti‐CD3 (clone 2C11) or 200 μg/mL BLG/OVA/PN and incubated at 37°C for 72 h. Butyrate inhibited IL‐4 (G) and IL‐13 (H) production and stimulated IL‐10 (I) and IFN‐γ (L) production in BLG‐, OVA‐, and PN‐sensitized mice. H 2 O 2 yield (M), SOD (N), and ROS‐induced damage on aconitase activity (O) were measured in hepatic mitochondria. The mitochondrial ROS‐induced dysfunction was proven by the higher mitochondrial H 2 O 2 yield, higher SOD activity, and lower basal/total aconitase ratio observed in all FA‐sensitized animals compared with the control group. Butyrate administration positively modulates the oxidative stress as demonstrated by the lower H 2 O 2 release, the decreased SOD activity, and the reactivation of the aconitase enzyme in all treated groups compared with control animals. Data are representative of at least 2 independent experiments, reported as median with range, and analyzed using the unpaired t test. BLG, mice sensitized with β‐lactoglobulin; CTRL, control mice; OVA, mice sensitized with ovalbumin; PN, mice sensitized with peanut extract. * P

    Techniques Used: Animal Model, Mouse Assay, Incubation, Activity Assay

    Evaluation of direct immunoregulatory action of HM butyrate on human peripheral blood mononuclear cells (PBMCs): Th2/Th1 and IL‐10 response and evaluation of FoxP3 expression. A, PBMCs from children with IgE‐mediated FA were stimulated with butyrate HM median concentration (0.75 mM) or with BLG, OVA, and PN (100 μL/well) in the presence or in the absence of butyrate HM median concentration for 24 h. BLG, OVA, and PN induced a significant increase in IL‐4 (A), IL‐5, and IL‐13 (C) production, but the presence of 0.75 mM butyrate significantly reduced the release of these Th2 cytokines. Butyrate alone or in the presence of specific allergen stimulated, at the same dose, IL‐10 (D) and IFN‐γ (E) production and FoxP3 expression (F), through a demethylation of respective gene (G, H, I) in CD4+ T cells purified from stimulated PBMCs from children with IgE‐mediated FA. (L) Butyrate treatment significantly reduced HDAC activity in a dose‐dependent manner in PBMCs. Data represent the median with range of 2 independent experiments, each performed in triplicate. Data were analyzed using the unpaired t test. BLG, β‐lactoglobulin; NT, untreated cells; OVA, ovalbumin; PN, peanut extracts. * P
    Figure Legend Snippet: Evaluation of direct immunoregulatory action of HM butyrate on human peripheral blood mononuclear cells (PBMCs): Th2/Th1 and IL‐10 response and evaluation of FoxP3 expression. A, PBMCs from children with IgE‐mediated FA were stimulated with butyrate HM median concentration (0.75 mM) or with BLG, OVA, and PN (100 μL/well) in the presence or in the absence of butyrate HM median concentration for 24 h. BLG, OVA, and PN induced a significant increase in IL‐4 (A), IL‐5, and IL‐13 (C) production, but the presence of 0.75 mM butyrate significantly reduced the release of these Th2 cytokines. Butyrate alone or in the presence of specific allergen stimulated, at the same dose, IL‐10 (D) and IFN‐γ (E) production and FoxP3 expression (F), through a demethylation of respective gene (G, H, I) in CD4+ T cells purified from stimulated PBMCs from children with IgE‐mediated FA. (L) Butyrate treatment significantly reduced HDAC activity in a dose‐dependent manner in PBMCs. Data represent the median with range of 2 independent experiments, each performed in triplicate. Data were analyzed using the unpaired t test. BLG, β‐lactoglobulin; NT, untreated cells; OVA, ovalbumin; PN, peanut extracts. * P

    Techniques Used: Expressing, Concentration Assay, Purification, Activity Assay

    Effects of HM butyrate in basal condition on gut barrier and on cytokine response. Four‐week‐old female C3H/HeJ mice were divided into two groups: (1) control mice (n = 4), receiving water as vehicle; (2) treated mice (n = 4), receiving oral butyrate once daily (30 mg/kg of body weight). After 14 d all mice were killed, and intestine, in particular ileum, jejunum, and colon, spleen, and mesenteric lymph nodes (MLN) were removed. A‐E, Oral butyrate treatment elicited a significant reduction in gut permeability, measured by plasma FITC‐dextran quantification, and increase in IL‐22, occludin, ZO‐1, and Muc2 expression. F‐L, Oral butyrate treatment induced a significant reduction in IL‐4, IL‐5, and IL‐13 and a significant increase in IFN‐γ and IL‐10 expression in MLN and spleen. M‐N, CD4+/CD25+/FoxP3+ cell numbers were increased after butyrate treatment in mouse spleen MLN and colon. Data are representative of at least 2 independent experiments, reported as median with range, and analyzed using the unpaired t test. * P
    Figure Legend Snippet: Effects of HM butyrate in basal condition on gut barrier and on cytokine response. Four‐week‐old female C3H/HeJ mice were divided into two groups: (1) control mice (n = 4), receiving water as vehicle; (2) treated mice (n = 4), receiving oral butyrate once daily (30 mg/kg of body weight). After 14 d all mice were killed, and intestine, in particular ileum, jejunum, and colon, spleen, and mesenteric lymph nodes (MLN) were removed. A‐E, Oral butyrate treatment elicited a significant reduction in gut permeability, measured by plasma FITC‐dextran quantification, and increase in IL‐22, occludin, ZO‐1, and Muc2 expression. F‐L, Oral butyrate treatment induced a significant reduction in IL‐4, IL‐5, and IL‐13 and a significant increase in IFN‐γ and IL‐10 expression in MLN and spleen. M‐N, CD4+/CD25+/FoxP3+ cell numbers were increased after butyrate treatment in mouse spleen MLN and colon. Data are representative of at least 2 independent experiments, reported as median with range, and analyzed using the unpaired t test. * P

    Techniques Used: Mouse Assay, Permeability, Expressing

    5) Product Images from "Pre-clinical study of human umbilical cord mesenchymal stem cell transplantation for the treatment of traumatic brain injury: safety evaluation from immunogenic and oncogenic perspectives"

    Article Title: Pre-clinical study of human umbilical cord mesenchymal stem cell transplantation for the treatment of traumatic brain injury: safety evaluation from immunogenic and oncogenic perspectives

    Journal: Neural Regeneration Research

    doi: 10.4103/1673-5374.317985

    Identification, immunogenicity and immunomodulation of huMSCs . (A) The huMSCs cultured in our experiment. The huMSCs were spindle-shaped and grew in a whorl pattern. Original magnification 100×, scale bars: 200 μm. (B) Flow cytometry detection of CD29, CD44, CD73 and CD105. The rate of positive expression for all factors was greater than 95%. (C) Detection of huMSC HLAII expression in PBMCs and huMSCs by western blot. No HLAII expression band was detected in the huMSCs. (D) Relative expression of HLAII in PBMCs and huMSCs. The bar graph shows no HLAII expression in huMSCs. (E) PCR amplification curves of HLA-DPA1 , HLA-DQA1 and HLA-DRA1 genes in PBMCs and huMSCs. (F) Relative expression of HLA-DPA1 , HLA-DQA1 and HLA-DRA1 genes in PBMCs and huMSCs. PCR results showed no expression of HLA-DPA1 , HLA-DQA1 or HLA-DRA1 genes in huMSCs. (G) Expression curves of serum IL-6, IL-10, IL-12, TGF-β, and TNF-α detected by ELISA method ( n = 5 rats per group). Compared with the TBI group, the serum pro-inflammatory cytokines IL-6, IL-12 and TNF-α in the Tail Vein and In Situ group were lower (### P
    Figure Legend Snippet: Identification, immunogenicity and immunomodulation of huMSCs . (A) The huMSCs cultured in our experiment. The huMSCs were spindle-shaped and grew in a whorl pattern. Original magnification 100×, scale bars: 200 μm. (B) Flow cytometry detection of CD29, CD44, CD73 and CD105. The rate of positive expression for all factors was greater than 95%. (C) Detection of huMSC HLAII expression in PBMCs and huMSCs by western blot. No HLAII expression band was detected in the huMSCs. (D) Relative expression of HLAII in PBMCs and huMSCs. The bar graph shows no HLAII expression in huMSCs. (E) PCR amplification curves of HLA-DPA1 , HLA-DQA1 and HLA-DRA1 genes in PBMCs and huMSCs. (F) Relative expression of HLA-DPA1 , HLA-DQA1 and HLA-DRA1 genes in PBMCs and huMSCs. PCR results showed no expression of HLA-DPA1 , HLA-DQA1 or HLA-DRA1 genes in huMSCs. (G) Expression curves of serum IL-6, IL-10, IL-12, TGF-β, and TNF-α detected by ELISA method ( n = 5 rats per group). Compared with the TBI group, the serum pro-inflammatory cytokines IL-6, IL-12 and TNF-α in the Tail Vein and In Situ group were lower (### P

    Techniques Used: Cell Culture, Flow Cytometry, Expressing, Western Blot, Polymerase Chain Reaction, Amplification, Enzyme-linked Immunosorbent Assay, In Situ

    6) Product Images from "Curcumin Modulates the Crosstalk Between Macrophages and Bone Mesenchymal Stem Cells to Ameliorate Osteogenesis"

    Article Title: Curcumin Modulates the Crosstalk Between Macrophages and Bone Mesenchymal Stem Cells to Ameliorate Osteogenesis

    Journal: Frontiers in Cell and Developmental Biology

    doi: 10.3389/fcell.2021.634650

    (A,B) Concentrations of IL-1β, TNF-α, IL-4, and IL-10 in the cell supernatant measured by ELISA. (C,D) Gene expressions of the pro-inflammatory cytokines IL-1β and TNF-α, and the anti-inflammatory cytokines IL-4 and IL-10 measured by real-time PCR. ∗∗ P
    Figure Legend Snippet: (A,B) Concentrations of IL-1β, TNF-α, IL-4, and IL-10 in the cell supernatant measured by ELISA. (C,D) Gene expressions of the pro-inflammatory cytokines IL-1β and TNF-α, and the anti-inflammatory cytokines IL-4 and IL-10 measured by real-time PCR. ∗∗ P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction

    7) Product Images from "Modulation of Wnt/β-catenin signaling in IL-17A-mediated macrophage polarization of RAW264.7 cells"

    Article Title: Modulation of Wnt/β-catenin signaling in IL-17A-mediated macrophage polarization of RAW264.7 cells

    Journal: Brazilian Journal of Medical and Biological Research

    doi: 10.1590/1414-431X20209488

    Production of cytokines in RAW264.7 cells in response to Wnt3A and/or interleukin (IL)-17 stimulation. A–C , Concentration of IL-6, tumor necrosis factor (TNF)-α, and IL-10 in culture media of cells treated with Wnt3A-CM and/or XAV939 without rhIL-17A or with rhIL-17A. **P
    Figure Legend Snippet: Production of cytokines in RAW264.7 cells in response to Wnt3A and/or interleukin (IL)-17 stimulation. A–C , Concentration of IL-6, tumor necrosis factor (TNF)-α, and IL-10 in culture media of cells treated with Wnt3A-CM and/or XAV939 without rhIL-17A or with rhIL-17A. **P

    Techniques Used: Concentration Assay

    8) Product Images from "A Critical Role of Autophagy in Regulating Microglia Polarization in Neurodegeneration"

    Article Title: A Critical Role of Autophagy in Regulating Microglia Polarization in Neurodegeneration

    Journal: Frontiers in Aging Neuroscience

    doi: 10.3389/fnagi.2018.00378

    Autophagy inhibition enhances M1 but reduces M2 markers in microglia. (A–D) qPCR measurement of M1 and M2 genes mRNA levels in TNF-α-treated cells with or without autophagy inhibition by 10 mM 3-MA ( A,B , primary microglia) or Atg5 knockdown ( C,D , BV2 microglial cell line). Atg5 siRNA or scrambled siRNA were transfected into BV2 cells by Lipofectamine RNAiMAX, followed by 5 ng/ml TNF-α treatment at 24 h later. mRNA levels were analyzed at 6 h after TNF-α addition. Graphs show relative mRNA levels after normalization with those of corresponding housekeeping gene 18 s. N = 3–6. (E–J) NO, IL-6 and IL-10 levels in the culture supernatants from TNF-α-treated microglia with 3-MA or Atg5 siRNA as described above, n = 4. (K) Western blot study of Atg5 expression in Atg5 siRNA-transfected BV2 cells following TNF-α treatment, n = 3. Housekeeping protein GAPDH was used as loading control for semi-quantitative densitometry. ∗ P
    Figure Legend Snippet: Autophagy inhibition enhances M1 but reduces M2 markers in microglia. (A–D) qPCR measurement of M1 and M2 genes mRNA levels in TNF-α-treated cells with or without autophagy inhibition by 10 mM 3-MA ( A,B , primary microglia) or Atg5 knockdown ( C,D , BV2 microglial cell line). Atg5 siRNA or scrambled siRNA were transfected into BV2 cells by Lipofectamine RNAiMAX, followed by 5 ng/ml TNF-α treatment at 24 h later. mRNA levels were analyzed at 6 h after TNF-α addition. Graphs show relative mRNA levels after normalization with those of corresponding housekeeping gene 18 s. N = 3–6. (E–J) NO, IL-6 and IL-10 levels in the culture supernatants from TNF-α-treated microglia with 3-MA or Atg5 siRNA as described above, n = 4. (K) Western blot study of Atg5 expression in Atg5 siRNA-transfected BV2 cells following TNF-α treatment, n = 3. Housekeeping protein GAPDH was used as loading control for semi-quantitative densitometry. ∗ P

    Techniques Used: Inhibition, Real-time Polymerase Chain Reaction, Transfection, Western Blot, Expressing

    A simplified summary of TNF-α induced autophagy flux inhibition and subsequent inflammation through AKT/mTOR signaling in microglia. TNF-α triggers the phosphorylation of AKT and mTOR, which plays a role in the autophagy flux disruption and causes a shift toward M1 phenotype in microglia. As a result, the microglia expression of the M1 markers such as iNOS/NO, IL-6, and IL-1β increases, while that of M2 genes including arginase, Ym1/2, and IL-10 decreases.
    Figure Legend Snippet: A simplified summary of TNF-α induced autophagy flux inhibition and subsequent inflammation through AKT/mTOR signaling in microglia. TNF-α triggers the phosphorylation of AKT and mTOR, which plays a role in the autophagy flux disruption and causes a shift toward M1 phenotype in microglia. As a result, the microglia expression of the M1 markers such as iNOS/NO, IL-6, and IL-1β increases, while that of M2 genes including arginase, Ym1/2, and IL-10 decreases.

    Techniques Used: Inhibition, Expressing

    Autophagy stimulation enhances M2 but reduces M1 markers in primary microglia. (A–F) qPCR analysis of M1 and M2 genes mRNA levels in TNF-α-treated primary microglia with or without autophagy stimulation by different methods. (A,B) 0.2 μg/ml rapamycin pretreatment. (C,D) serum deprivation. (E,F) autophagy stimulation by 50 μM resveratrol pretreatment. Graphs show relative mRNA levels after normalization with those of corresponding housekeeping gene 18 s, n = 4. (G–I) Cytokines including NO (G) , IL-6 (H) and IL-10 levels (I) , measured by Griess reagent and ELISA, in cell-free culture supernatant from TNF-α-challenged primary microglia with or without rapamycin pretreatment. N = 4. All of the results are expressed as mean ± SEM, one-way ANOVA followed by Tukey analysis. ∗ P
    Figure Legend Snippet: Autophagy stimulation enhances M2 but reduces M1 markers in primary microglia. (A–F) qPCR analysis of M1 and M2 genes mRNA levels in TNF-α-treated primary microglia with or without autophagy stimulation by different methods. (A,B) 0.2 μg/ml rapamycin pretreatment. (C,D) serum deprivation. (E,F) autophagy stimulation by 50 μM resveratrol pretreatment. Graphs show relative mRNA levels after normalization with those of corresponding housekeeping gene 18 s, n = 4. (G–I) Cytokines including NO (G) , IL-6 (H) and IL-10 levels (I) , measured by Griess reagent and ELISA, in cell-free culture supernatant from TNF-α-challenged primary microglia with or without rapamycin pretreatment. N = 4. All of the results are expressed as mean ± SEM, one-way ANOVA followed by Tukey analysis. ∗ P

    Techniques Used: Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    9) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    10) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    11) Product Images from "The Relationship between Th1/Th2 Balance and 1α, 25-Dihydroxyvitamin D3 in Patients with Allergic Rhinitis"

    Article Title: The Relationship between Th1/Th2 Balance and 1α, 25-Dihydroxyvitamin D3 in Patients with Allergic Rhinitis

    Journal: Turkish Archives of Otorhinolaryngology

    doi: 10.5152/tao.2015.1187

    Correlation between vitamin D and IL-10 in the study group
    Figure Legend Snippet: Correlation between vitamin D and IL-10 in the study group

    Techniques Used:

    12) Product Images from "Aryl Hydrocarbon Receptor Promotes IL-10 Expression in Inflammatory Macrophages Through Src-STAT3 Signaling Pathway"

    Article Title: Aryl Hydrocarbon Receptor Promotes IL-10 Expression in Inflammatory Macrophages Through Src-STAT3 Signaling Pathway

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2018.02033

    AhR upregulated LPS-induced IL-10 expression through Src pathway in macrophages. (A,B) RAW/NC and RAW/AhR cells were untreated or treated with LPS for 1 h and cell lysates then subjected to western blotting analysis with anti-phosphotyrosine Src and Src antibodies. (B) Densitometric analysis of relative abundances of phospho-Src normalized to total Src. Combined results are compared using one-way ANOVA test ( n = 3; control, P = 0.012; LPS, P = 0.039). (C–F) Cells were pre-treated with two different Src inhibitors (PP2 and dasatinib) for 1 h and then stimulated with or without LPS for the indicated times. (C,D) Whole-cell extracts were immunoblotted with specific antibodies. (E) IL-10 mRNA levels were detected with qRT-PCR. Combined results are compared using one-way ANOVA test ( n = 3; PP2, P = 0.015). (F) IL-10 protein levels were detected with ELISA. Combined results are compared using one-way ANOVA test ( n = 3; PP2, P = 0.003; dasatinib, P = 0.002). (G,H) Cells were transfected with scrambled or Src-specific siRNA and then incubated with or without LPS for 12 h. Whole-cell lysates were subjected to western blotting analysis. Combined results are compared using one-way ANOVA test ( n = 4; siSrc-1, P = 0.003; siSrc-2, P = 0.004). IL-10 levels in the supernatant were determined with ELISA. Combined results are compared using one-way ANOVA test (n = 3; siSrc-1, P = 0.011; siSrc-2, P = 0.011). (I) Peritoneal macrophages isolated from WT or AhR-KO mice were stimulated with or without LPS for 6 h. Whole-cell lysates were subjected to western blot analysis. Western blot images are representative of three independent experiments. Data in all bar graphs are mean ± SEM of three independent experiments. Differences were analyzed with one-way ANOVA. * P
    Figure Legend Snippet: AhR upregulated LPS-induced IL-10 expression through Src pathway in macrophages. (A,B) RAW/NC and RAW/AhR cells were untreated or treated with LPS for 1 h and cell lysates then subjected to western blotting analysis with anti-phosphotyrosine Src and Src antibodies. (B) Densitometric analysis of relative abundances of phospho-Src normalized to total Src. Combined results are compared using one-way ANOVA test ( n = 3; control, P = 0.012; LPS, P = 0.039). (C–F) Cells were pre-treated with two different Src inhibitors (PP2 and dasatinib) for 1 h and then stimulated with or without LPS for the indicated times. (C,D) Whole-cell extracts were immunoblotted with specific antibodies. (E) IL-10 mRNA levels were detected with qRT-PCR. Combined results are compared using one-way ANOVA test ( n = 3; PP2, P = 0.015). (F) IL-10 protein levels were detected with ELISA. Combined results are compared using one-way ANOVA test ( n = 3; PP2, P = 0.003; dasatinib, P = 0.002). (G,H) Cells were transfected with scrambled or Src-specific siRNA and then incubated with or without LPS for 12 h. Whole-cell lysates were subjected to western blotting analysis. Combined results are compared using one-way ANOVA test ( n = 4; siSrc-1, P = 0.003; siSrc-2, P = 0.004). IL-10 levels in the supernatant were determined with ELISA. Combined results are compared using one-way ANOVA test (n = 3; siSrc-1, P = 0.011; siSrc-2, P = 0.011). (I) Peritoneal macrophages isolated from WT or AhR-KO mice were stimulated with or without LPS for 6 h. Whole-cell lysates were subjected to western blot analysis. Western blot images are representative of three independent experiments. Data in all bar graphs are mean ± SEM of three independent experiments. Differences were analyzed with one-way ANOVA. * P

    Techniques Used: Expressing, Western Blot, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Transfection, Incubation, Isolation, Mouse Assay

    Proposed network for AhR-Src-STAT3-IL-10 signaling pathway in inflammatory macrophages. AhR expression is highly enhanced in LPS-induced inflammatory macrophages via the NF-κB pathway. AhR binds to the IL-10-promoter, but does not affect the transcriptional activity of IL-10. Increased AhR in the cytoplasm upregulates the tyrosine phosphorylation of Src, which can be suppressed by selective Src inhibitors (PP2 and dasatinib). STAT3 is also activated by phosphorylation of tyrosine 705, triggered by Src tyrosine kinase and suppressed by selective STAT3 inhibitors (cryptotanshinone and BP-1-102). STAT3 activation is independent of IL-10 autocrine feedback, Akt/mTOR, and MAPK pathways. The activated signaling pathway promotes LPS-induced IL-10 expression. Overall, AhR-associated Src activity is responsible for the tyrosine phosphorylation of STAT3 and IL-10 expression in LPS-induced inflammatory macrophages.
    Figure Legend Snippet: Proposed network for AhR-Src-STAT3-IL-10 signaling pathway in inflammatory macrophages. AhR expression is highly enhanced in LPS-induced inflammatory macrophages via the NF-κB pathway. AhR binds to the IL-10-promoter, but does not affect the transcriptional activity of IL-10. Increased AhR in the cytoplasm upregulates the tyrosine phosphorylation of Src, which can be suppressed by selective Src inhibitors (PP2 and dasatinib). STAT3 is also activated by phosphorylation of tyrosine 705, triggered by Src tyrosine kinase and suppressed by selective STAT3 inhibitors (cryptotanshinone and BP-1-102). STAT3 activation is independent of IL-10 autocrine feedback, Akt/mTOR, and MAPK pathways. The activated signaling pathway promotes LPS-induced IL-10 expression. Overall, AhR-associated Src activity is responsible for the tyrosine phosphorylation of STAT3 and IL-10 expression in LPS-induced inflammatory macrophages.

    Techniques Used: Expressing, Activity Assay, Activation Assay

    Loss of AhR in macrophages reduced IL-10 expression after LPS stimulation. Peritoneal macrophages and BMDMs isolated from WT or AhR-KO mice were stimulated with or without LPS at the indicated time points. (A,B) Whole-cell lysates were subjected to western blotting analysis with anti-AhR antibody. (C,D) IL-10 mRNA levels were detected with qRT-PCR at 4 h after LPS stimulation. The experiment was repeated three times; combined results are compared using one-way ANOVA test (PMs, P
    Figure Legend Snippet: Loss of AhR in macrophages reduced IL-10 expression after LPS stimulation. Peritoneal macrophages and BMDMs isolated from WT or AhR-KO mice were stimulated with or without LPS at the indicated time points. (A,B) Whole-cell lysates were subjected to western blotting analysis with anti-AhR antibody. (C,D) IL-10 mRNA levels were detected with qRT-PCR at 4 h after LPS stimulation. The experiment was repeated three times; combined results are compared using one-way ANOVA test (PMs, P

    Techniques Used: Expressing, Isolation, Mouse Assay, Western Blot, Quantitative RT-PCR

    AhR upregulated LPS-induced IL-10 expression in RAW264.7 cells independent of AhR genomic pathway. AhR and Flag protein (A) and mRNA (B) levels were detected in RAW, RAW/NC, and RAW/AhR cells. The experiment was repeated three times; combined results are compared using one-way ANOVA test (RAW/NC, P
    Figure Legend Snippet: AhR upregulated LPS-induced IL-10 expression in RAW264.7 cells independent of AhR genomic pathway. AhR and Flag protein (A) and mRNA (B) levels were detected in RAW, RAW/NC, and RAW/AhR cells. The experiment was repeated three times; combined results are compared using one-way ANOVA test (RAW/NC, P

    Techniques Used: Expressing

    Maximal IL-10 production was associated with STAT3-activation in LPS-induced AhR-overexpressing macrophages. RAW/NC and RAW/AhR cells were untreated or treated with LPS. (A–C) Cells were stimulated with LPS for 1 h and cell lysates were used for western blotting analysis with anti-phosphotyrosine STAT3, phosphoserine STAT3, STAT3, and AhR antibodies. (B,C) Densitometric analysis of relative abundance of phosphotyrosine-STAT3 and phosphoserine-STAT3 normalized to total STAT3. The experiment was repeated three times; combined results are compared using one-way ANOVA test ( P = 0.020). (D) Cells were pre-treated with IL-10-blocking antibody (1 μg/ml) for 12 h and then stimulated with LPS for 1 h, followed by western blotting of whole-cell extracts. (E,F) Cells were transfected with scrambled or STAT3-specific siRNA and then incubated with or without LPS for 12 h. Whole-cell lysates were subjected to western blotting analysis. Combined results are compared using one-way ANOVA test ( n = 3; siSTAT3-1, P = 0.015; siSTAT3-2, P = 0.039). IL-10 levels in the supernatant were determined with ELISA. Combined results are compared using one-way ANOVA test ( n = 3; siSTAT3-1, P = 0.004; siSTAT3-2, P = 0.009). (G–I) Cells were pre-treated with two different STAT3 inhibitors (cryptotanshinone and BP-1-102) for 1 h and then stimulated with or without LPS for the indicated times. (G) Whole-cell extracts were immunoblotted with anti-phosphotyrosine STAT3 and STAT3 antibodies. (H) IL-10 mRNA levels were detected with qRT-PCR. Combined results are compared using one-way ANOVA test ( n = 3; cryptotanshinone, P = 0.017; BP-1-102, P = 0.010). (I) IL-10 protein levels were detected with ELISA. Combined results are compared using one-way ANOVA test ( n = 3; cryptotanshinone, P = 0.004; BP-1-102, P = 0.002). Western blot images are representative of three independent experiments. Data in all bar graphs are mean ± SEM of three independent experiments. Differences were analyzed with one-way ANOVA. * P
    Figure Legend Snippet: Maximal IL-10 production was associated with STAT3-activation in LPS-induced AhR-overexpressing macrophages. RAW/NC and RAW/AhR cells were untreated or treated with LPS. (A–C) Cells were stimulated with LPS for 1 h and cell lysates were used for western blotting analysis with anti-phosphotyrosine STAT3, phosphoserine STAT3, STAT3, and AhR antibodies. (B,C) Densitometric analysis of relative abundance of phosphotyrosine-STAT3 and phosphoserine-STAT3 normalized to total STAT3. The experiment was repeated three times; combined results are compared using one-way ANOVA test ( P = 0.020). (D) Cells were pre-treated with IL-10-blocking antibody (1 μg/ml) for 12 h and then stimulated with LPS for 1 h, followed by western blotting of whole-cell extracts. (E,F) Cells were transfected with scrambled or STAT3-specific siRNA and then incubated with or without LPS for 12 h. Whole-cell lysates were subjected to western blotting analysis. Combined results are compared using one-way ANOVA test ( n = 3; siSTAT3-1, P = 0.015; siSTAT3-2, P = 0.039). IL-10 levels in the supernatant were determined with ELISA. Combined results are compared using one-way ANOVA test ( n = 3; siSTAT3-1, P = 0.004; siSTAT3-2, P = 0.009). (G–I) Cells were pre-treated with two different STAT3 inhibitors (cryptotanshinone and BP-1-102) for 1 h and then stimulated with or without LPS for the indicated times. (G) Whole-cell extracts were immunoblotted with anti-phosphotyrosine STAT3 and STAT3 antibodies. (H) IL-10 mRNA levels were detected with qRT-PCR. Combined results are compared using one-way ANOVA test ( n = 3; cryptotanshinone, P = 0.017; BP-1-102, P = 0.010). (I) IL-10 protein levels were detected with ELISA. Combined results are compared using one-way ANOVA test ( n = 3; cryptotanshinone, P = 0.004; BP-1-102, P = 0.002). Western blot images are representative of three independent experiments. Data in all bar graphs are mean ± SEM of three independent experiments. Differences were analyzed with one-way ANOVA. * P

    Techniques Used: Activation Assay, Western Blot, Blocking Assay, Transfection, Incubation, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

    Adoptive transfer of AhR-expressing peritoneal macrophages protected mice against LPS-induced peritonitis. (A) Flow cytometry profiles of peritoneal macrophages after 36 h incubation with AhR-overexpressing adenovirus (Ad-AhR) or negative control adenovirus (Ad-NC). (B–E) Peritoneal macrophages from AhR-KO (B,C) and WT (D,E) mice were transfected with Ad-AhR or Ad-NC and then incubated with or without LPS for 12 h. Whole-cell lysates were subjected to western blotting analysis and IL-10 levels in the supernatant were determined with ELISA. Combined results are compared using one-way ANOVA test ( n = 3; AhR-KO, P
    Figure Legend Snippet: Adoptive transfer of AhR-expressing peritoneal macrophages protected mice against LPS-induced peritonitis. (A) Flow cytometry profiles of peritoneal macrophages after 36 h incubation with AhR-overexpressing adenovirus (Ad-AhR) or negative control adenovirus (Ad-NC). (B–E) Peritoneal macrophages from AhR-KO (B,C) and WT (D,E) mice were transfected with Ad-AhR or Ad-NC and then incubated with or without LPS for 12 h. Whole-cell lysates were subjected to western blotting analysis and IL-10 levels in the supernatant were determined with ELISA. Combined results are compared using one-way ANOVA test ( n = 3; AhR-KO, P

    Techniques Used: Adoptive Transfer Assay, Expressing, Mouse Assay, Flow Cytometry, Incubation, Negative Control, Transfection, Western Blot, Enzyme-linked Immunosorbent Assay

    13) Product Images from "Tropomodulin1 Expression Increases Upon Maturation in Dendritic Cells and Promotes Their Maturation and Immune Functions"

    Article Title: Tropomodulin1 Expression Increases Upon Maturation in Dendritic Cells and Promotes Their Maturation and Immune Functions

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2020.587441

    Exogenous Tmod1 expression reversed the effect of Tmod1 deficiency on Toll-like receptor 4 (TLR4) signaling. (A) Immature dendritic cells (ImDCs) from TOT/Tmod1 -/- mice were infected with Tmod1 adenovirus (Ad-Tmod1) or control adenovirus (Ad-Null) at 200 multiplicity of infection (MOI) for 6 h. ImDCs without adenovirus treatment were used as the negative control (-). Adenovirus infected or un-infected imDCs were further treated with LPS (100 ng/ml) for 24 h and total RNAs were extracted. The mRNA expression of Tmod1 , MyD88 downstream genes ( CD86 , Il6 , Tnfa , and Il12 ) and TRIF/IRF3 downstream gene ( Il10 ) were detected by qPCR. (B, C) Culture media were collected at the end of lipopolysaccharide (LPS) treatment. The concentrations of cytokines, TNF-α (B) and IL-10 (C) , were measured by ELISA kits. Data are presented as mean ± SEM. *p
    Figure Legend Snippet: Exogenous Tmod1 expression reversed the effect of Tmod1 deficiency on Toll-like receptor 4 (TLR4) signaling. (A) Immature dendritic cells (ImDCs) from TOT/Tmod1 -/- mice were infected with Tmod1 adenovirus (Ad-Tmod1) or control adenovirus (Ad-Null) at 200 multiplicity of infection (MOI) for 6 h. ImDCs without adenovirus treatment were used as the negative control (-). Adenovirus infected or un-infected imDCs were further treated with LPS (100 ng/ml) for 24 h and total RNAs were extracted. The mRNA expression of Tmod1 , MyD88 downstream genes ( CD86 , Il6 , Tnfa , and Il12 ) and TRIF/IRF3 downstream gene ( Il10 ) were detected by qPCR. (B, C) Culture media were collected at the end of lipopolysaccharide (LPS) treatment. The concentrations of cytokines, TNF-α (B) and IL-10 (C) , were measured by ELISA kits. Data are presented as mean ± SEM. *p

    Techniques Used: Expressing, Mouse Assay, Infection, Negative Control, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    Tmod1 deficiency promotes the activation of TRIF-dependent pathway and expression of type I interferons in dendritic cells (DCs). (A) The immature DC (imDCs) from Tmod1 +/+ and TOT/Tmod1 -/- mice were treated with LPS (100 ng/ml) for 0, 2, 4, 6 h, respectively, and then total proteins were extracted. The expression of phosphorylated IRF3 (p-IRF3) and total IRF3 (t-IRF3) were detected by western blotting. GAPDH were used as an internal control. (B) The expressions of p-IRF3 at different time points were quantified after normalization to t-IRF3 and the data was presented as fold change. (C) The imDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice were matured by LPS treatment for 2 days. Total RNAs were extracted from imDCs and mature DCs (mDCs) of both genotypes and qPCR was performed to detect the expression of IFN-β ( Ifnb ) and IL-10 ( Il10 ). (D) Culture media were collected from lipopolysaccharide (LPS)-induced mDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice. The concentrations of IFN-β and IL-10 were measured on a flow cytometer by using a bead-based immunoassay kit. Data are presented as mean ± SEM. *p
    Figure Legend Snippet: Tmod1 deficiency promotes the activation of TRIF-dependent pathway and expression of type I interferons in dendritic cells (DCs). (A) The immature DC (imDCs) from Tmod1 +/+ and TOT/Tmod1 -/- mice were treated with LPS (100 ng/ml) for 0, 2, 4, 6 h, respectively, and then total proteins were extracted. The expression of phosphorylated IRF3 (p-IRF3) and total IRF3 (t-IRF3) were detected by western blotting. GAPDH were used as an internal control. (B) The expressions of p-IRF3 at different time points were quantified after normalization to t-IRF3 and the data was presented as fold change. (C) The imDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice were matured by LPS treatment for 2 days. Total RNAs were extracted from imDCs and mature DCs (mDCs) of both genotypes and qPCR was performed to detect the expression of IFN-β ( Ifnb ) and IL-10 ( Il10 ). (D) Culture media were collected from lipopolysaccharide (LPS)-induced mDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice. The concentrations of IFN-β and IL-10 were measured on a flow cytometer by using a bead-based immunoassay kit. Data are presented as mean ± SEM. *p

    Techniques Used: Activation Assay, Expressing, Mouse Assay, Western Blot, Real-time Polymerase Chain Reaction, Flow Cytometry, Bead-based Assay

    Tmod1 deficiency impaired the T-cell stimulatory ability of mature dendritic cells (mDCs) and induced immune tolerance in the experimental autoimmune encephalomyelitis (EAE) model. (A) LPS-induced mDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice were incubated with 1×10 5 T cells in 1:100, 1:10, 1:1 ratios in the mixed lymphocytes reaction. The proliferation of T cells was measured by cell counting kit-8 and optical densities at 450 nm (OD450) were obtained. (B, C) Lipopolysaccharide (LPS)-induced mDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice (N=5) were treated with OVA peptide (323-339) and then transfused, respectively, to C57BL/6J mice at day 1, 3, and 5. On day 8, the spleen cells of transfused mice were collected and stimulated with OVA peptide (323-339) for another 3 days. The stimulated spleen cells were stained with FITC-conjugated anti-CD4 antibody or isotype control and analyzed by flow cytometry. The representative histograms were presented (B) and the percentages of CD4 + T cells were obtained (C) . (D) The culture media of OVA peptide-stimulated spleen cells were collected and the concentrations of IL-10 and IFN-γ were measured on a flow cytometer by using a bead-based immunoassay kit. (E) LPS-induced mDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice (N=5) were pulsed with MOG35-55 peptide and transfused, respectively, to C57BL/6J mice on day 0 and day 4. EAE was induced by injection of MOG35-55 peptide and Mycobacterium tuberculosis on day 7 and 14, and pertussis toxin on day 7 and 9. The mice were observed and scored from day 14 until day 44. The mean disease scores were plotted. Data are presented as mean ± SEM. *p
    Figure Legend Snippet: Tmod1 deficiency impaired the T-cell stimulatory ability of mature dendritic cells (mDCs) and induced immune tolerance in the experimental autoimmune encephalomyelitis (EAE) model. (A) LPS-induced mDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice were incubated with 1×10 5 T cells in 1:100, 1:10, 1:1 ratios in the mixed lymphocytes reaction. The proliferation of T cells was measured by cell counting kit-8 and optical densities at 450 nm (OD450) were obtained. (B, C) Lipopolysaccharide (LPS)-induced mDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice (N=5) were treated with OVA peptide (323-339) and then transfused, respectively, to C57BL/6J mice at day 1, 3, and 5. On day 8, the spleen cells of transfused mice were collected and stimulated with OVA peptide (323-339) for another 3 days. The stimulated spleen cells were stained with FITC-conjugated anti-CD4 antibody or isotype control and analyzed by flow cytometry. The representative histograms were presented (B) and the percentages of CD4 + T cells were obtained (C) . (D) The culture media of OVA peptide-stimulated spleen cells were collected and the concentrations of IL-10 and IFN-γ were measured on a flow cytometer by using a bead-based immunoassay kit. (E) LPS-induced mDCs from Tmod1 +/+ and TOT/Tmod1 -/- mice (N=5) were pulsed with MOG35-55 peptide and transfused, respectively, to C57BL/6J mice on day 0 and day 4. EAE was induced by injection of MOG35-55 peptide and Mycobacterium tuberculosis on day 7 and 14, and pertussis toxin on day 7 and 9. The mice were observed and scored from day 14 until day 44. The mean disease scores were plotted. Data are presented as mean ± SEM. *p

    Techniques Used: Mouse Assay, Incubation, Cell Counting, Staining, Flow Cytometry, Bead-based Assay, Injection

    14) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    15) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    16) Product Images from "Lentivirus-mediated downregulation of α-synuclein reduces neuroinflammation and promotes functional recovery in rats with spinal cord injury"

    Article Title: Lentivirus-mediated downregulation of α-synuclein reduces neuroinflammation and promotes functional recovery in rats with spinal cord injury

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-019-1658-2

    Knockdown of α-Syn promotes changes in peripheral serum inflammation after SCI. a – d Changes in the levels of the pro-inflammatory cytokines IL-1β, IL-2, TNF-α, and IFN-γ, n = 13. e – g Changes in the levels of the anti-inflammatory cytokines IL-10, IL-4, and TGF-β1, n = 13. All data are presented as the mean ± SD. One-way ANOVA and Tukey’s multiple comparisons test were used to analyse differences among groups
    Figure Legend Snippet: Knockdown of α-Syn promotes changes in peripheral serum inflammation after SCI. a – d Changes in the levels of the pro-inflammatory cytokines IL-1β, IL-2, TNF-α, and IFN-γ, n = 13. e – g Changes in the levels of the anti-inflammatory cytokines IL-10, IL-4, and TGF-β1, n = 13. All data are presented as the mean ± SD. One-way ANOVA and Tukey’s multiple comparisons test were used to analyse differences among groups

    Techniques Used:

    Reduced α-Syn levels significantly increase Arg1 expression in microglia/macrophages. A Representative images showing Iba1+/Arg1+ IF staining after SCI (a, e, and i show microglia (Iba1); b, f, and j show iNOS; and c, j, and k show cell nuclei (DAPI)). Scale bar = 100 μm. B Quantitative analysis of the results in panel B , n = 5. C , D Relative mRNA expression levels of CD206 and IL-10 in all groups, as detected by qRT-PCR. All data are presented as the mean ± SD, n = 5. One-way ANOVA and Tukey’s multiple comparisons test were used to analyse differences among groups
    Figure Legend Snippet: Reduced α-Syn levels significantly increase Arg1 expression in microglia/macrophages. A Representative images showing Iba1+/Arg1+ IF staining after SCI (a, e, and i show microglia (Iba1); b, f, and j show iNOS; and c, j, and k show cell nuclei (DAPI)). Scale bar = 100 μm. B Quantitative analysis of the results in panel B , n = 5. C , D Relative mRNA expression levels of CD206 and IL-10 in all groups, as detected by qRT-PCR. All data are presented as the mean ± SD, n = 5. One-way ANOVA and Tukey’s multiple comparisons test were used to analyse differences among groups

    Techniques Used: Expressing, Staining, Quantitative RT-PCR

    17) Product Images from "Platelet-rich plasma plays an antibacterial, anti-inflammatory and cell proliferation-promoting role in an in vitro model for diabetic infected wounds"

    Article Title: Platelet-rich plasma plays an antibacterial, anti-inflammatory and cell proliferation-promoting role in an in vitro model for diabetic infected wounds

    Journal: Infection and Drug Resistance

    doi: 10.2147/IDR.S186651

    ( A ) IL-6, ( B ) IL-10, ( C ) TNF-α, ( D ) TGF-β1 content in the supernatant as determined by ELISA. Notes: Significant deviations from the HaCaT control at the respective incubation time (* P
    Figure Legend Snippet: ( A ) IL-6, ( B ) IL-10, ( C ) TNF-α, ( D ) TGF-β1 content in the supernatant as determined by ELISA. Notes: Significant deviations from the HaCaT control at the respective incubation time (* P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Incubation

    ( A ) IL-6, ( B ) IL-10, ( C ) TNF-α, ( D ) TGF-β1 mRNA expression in HaCaT cells as measured by qRT-PCR. Notes: In the setting of bacterial infection, results at the 48th hour are not shown because of insufficient RNA extracted from residual cells. Significant deviations from the HaCaT control at the respective incubation time (* P
    Figure Legend Snippet: ( A ) IL-6, ( B ) IL-10, ( C ) TNF-α, ( D ) TGF-β1 mRNA expression in HaCaT cells as measured by qRT-PCR. Notes: In the setting of bacterial infection, results at the 48th hour are not shown because of insufficient RNA extracted from residual cells. Significant deviations from the HaCaT control at the respective incubation time (* P

    Techniques Used: Expressing, Quantitative RT-PCR, Infection, Incubation

    18) Product Images from "The Therapeutic Effects of Exosomes Derived from Human Umbilical Cord Mesenchymal Stem Cells on Scleroderma"

    Article Title: The Therapeutic Effects of Exosomes Derived from Human Umbilical Cord Mesenchymal Stem Cells on Scleroderma

    Journal: Tissue Engineering and Regenerative Medicine

    doi: 10.1007/s13770-021-00405-5

    HUMSCs-Ex modulated the balance of M1/M2 macrophages. A – D The ELISA results of the inflammatory cytokines IL-6, IL-12, IL-4 and IL-10 in serum. E – H The ratio of IL-6/IL-4, IL-6/IL-10, IL-12/IL-4 and IL-12/IL-10 protein. I – K Western blot and quantification of iNOS and Arg-1 in skin. L The ratio of iNOS/Arg-1 protein. M – P Skin sections were stained with anti-F4/80 together with anti-iNOS or anti-CD206. Scale bars = 20 μm. The number of double-positive cells was counted under each high power field. Data are presented as the mean ± SD, * p
    Figure Legend Snippet: HUMSCs-Ex modulated the balance of M1/M2 macrophages. A – D The ELISA results of the inflammatory cytokines IL-6, IL-12, IL-4 and IL-10 in serum. E – H The ratio of IL-6/IL-4, IL-6/IL-10, IL-12/IL-4 and IL-12/IL-10 protein. I – K Western blot and quantification of iNOS and Arg-1 in skin. L The ratio of iNOS/Arg-1 protein. M – P Skin sections were stained with anti-F4/80 together with anti-iNOS or anti-CD206. Scale bars = 20 μm. The number of double-positive cells was counted under each high power field. Data are presented as the mean ± SD, * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Western Blot, Staining

    19) Product Images from "Isovitexin-Mediated Regulation of Microglial Polarization in Lipopolysaccharide-Induced Neuroinflammation via Activation of the CaMKKβ/AMPK-PGC-1α Signaling Axis"

    Article Title: Isovitexin-Mediated Regulation of Microglial Polarization in Lipopolysaccharide-Induced Neuroinflammation via Activation of the CaMKKβ/AMPK-PGC-1α Signaling Axis

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2019.02650

    IVX-mediated CaMKKβ activation inhibited M1 microglial polarization and promoted M2 microglial polarization in the cerebral cortices of LPS-injected mice. After the open field test, the cerebral cortices of mice were harvested. To investigate the effect of IVX-mediated CaMKKβ activation on microglial polarization in LPS-injected mice, the mRNA and protein expression of M1 microglial markers (TNF-α and iNOS) and M2 microglial markers (Arg-1 and CD206) were detected via RT-PCR and western blotting. (A,B) The mRNA expression of M1 microglial markers (TNF-α and iNOS) were measured via RT-PCR. (C,D) The mRNA expression of M2 microglial markers (Arg-1 and CD206) was measured via RT-PCR. (F–H) The protein expression of M1 microglial markers (TNF-α and iNOS) were measured via western blotting. (I,J) The protein expression of M2 microglial markers (Arg-1 and CD206) was measured via western blotting. (E,K) The gene and protein expression of IL-10 was measured via RT-PCR and western blotting. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4–5 in each group). # p
    Figure Legend Snippet: IVX-mediated CaMKKβ activation inhibited M1 microglial polarization and promoted M2 microglial polarization in the cerebral cortices of LPS-injected mice. After the open field test, the cerebral cortices of mice were harvested. To investigate the effect of IVX-mediated CaMKKβ activation on microglial polarization in LPS-injected mice, the mRNA and protein expression of M1 microglial markers (TNF-α and iNOS) and M2 microglial markers (Arg-1 and CD206) were detected via RT-PCR and western blotting. (A,B) The mRNA expression of M1 microglial markers (TNF-α and iNOS) were measured via RT-PCR. (C,D) The mRNA expression of M2 microglial markers (Arg-1 and CD206) was measured via RT-PCR. (F–H) The protein expression of M1 microglial markers (TNF-α and iNOS) were measured via western blotting. (I,J) The protein expression of M2 microglial markers (Arg-1 and CD206) was measured via western blotting. (E,K) The gene and protein expression of IL-10 was measured via RT-PCR and western blotting. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4–5 in each group). # p

    Techniques Used: Activation Assay, Injection, Mouse Assay, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot

    PPARγ activation is involved in IVX-mediated microglial polarization in LPS- induced BV-2 cells and mouse primary microglia. (A) After treatment with T0070907 (an inhibitor of PPARγ) for 2 h and PPARγ siRNA for 24 h and then IVX for 2 h in BV-2 cells and mouse primary microglia, the protein expression of PPARγ was measured with Western blotting. Following pretreatment with 5 μM T0070907 for 2 h and PPARγ siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 6 h. (E) The protein expression of PPARγ was detected via Western blotting. (B,F) The mRNA expression of M2 microglial markers (Arg-1, CD206, and YM1/2) were detected via RT-PCR. (D,H) The mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) were detected via RT-PCR. Pretreatment with 5 μM T0070907 for 2 h and PPARγ siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 24 h. (C,G) The release of IL-10 was measured with ELISA. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4 in each group). ## p
    Figure Legend Snippet: PPARγ activation is involved in IVX-mediated microglial polarization in LPS- induced BV-2 cells and mouse primary microglia. (A) After treatment with T0070907 (an inhibitor of PPARγ) for 2 h and PPARγ siRNA for 24 h and then IVX for 2 h in BV-2 cells and mouse primary microglia, the protein expression of PPARγ was measured with Western blotting. Following pretreatment with 5 μM T0070907 for 2 h and PPARγ siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 6 h. (E) The protein expression of PPARγ was detected via Western blotting. (B,F) The mRNA expression of M2 microglial markers (Arg-1, CD206, and YM1/2) were detected via RT-PCR. (D,H) The mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) were detected via RT-PCR. Pretreatment with 5 μM T0070907 for 2 h and PPARγ siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 24 h. (C,G) The release of IL-10 was measured with ELISA. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4 in each group). ## p

    Techniques Used: Activation Assay, Expressing, Western Blot, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    PGC-1α activation is involved in IVX-mediated microglial polarization in LPS- induced BV-2 cells and mouse primary microglia. (A) After treatment with SR-18292 (an inhibitor of PGC-1α) for 3 h and PGC-1α siRNA for 24 h and then IVX for 2 h in BV-2 cells and mouse primary microglia, the protein expression of PGC-1α was measured with Western blotting. Following pretreatment with 2.5 μM SR-18292 for 3 h and PGC-1α siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 6 h. (E) The protein expression of PGC-1α was detected via Western blotting. (B,F) The mRNA expression of M2 microglial markers (Arg-1, CD206, and YM1/2) were detected via RT-PCR. (D,H) The mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) were detected via RT-PCR. Pretreatment with 2.5 μM SR-18292 for 3 h and PGC-1α siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 24 h. (C,G) The release of IL-10 was measured with ELISA. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4 in each group). ## p
    Figure Legend Snippet: PGC-1α activation is involved in IVX-mediated microglial polarization in LPS- induced BV-2 cells and mouse primary microglia. (A) After treatment with SR-18292 (an inhibitor of PGC-1α) for 3 h and PGC-1α siRNA for 24 h and then IVX for 2 h in BV-2 cells and mouse primary microglia, the protein expression of PGC-1α was measured with Western blotting. Following pretreatment with 2.5 μM SR-18292 for 3 h and PGC-1α siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 6 h. (E) The protein expression of PGC-1α was detected via Western blotting. (B,F) The mRNA expression of M2 microglial markers (Arg-1, CD206, and YM1/2) were detected via RT-PCR. (D,H) The mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) were detected via RT-PCR. Pretreatment with 2.5 μM SR-18292 for 3 h and PGC-1α siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 24 h. (C,G) The release of IL-10 was measured with ELISA. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4 in each group). ## p

    Techniques Used: Pyrolysis Gas Chromatography, Activation Assay, Expressing, Western Blot, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    CaMKKβ activation is involved in IVX-mediated microglial polarization in BV-2 cells and mouse primary microglia. (D) After treatment with CaMKKβ siRNA for 24 h and then IVX for 2 h in mouse primary microglia, the protein expression of CaMKKβ was measured with Western blotting. (E) After treated with CaMKKβ siRNA for 24 h, mouse primary microglia were exposed to IVX for 1 h. The protein expression of p-AMPK was detected by Western blotting. (F) After treated with CaMKKβ siRNA for 24 h, mouse primary microglia were exposed to IVX for 3 h. The protein expression of PGC-1α was detected by Western blotting. Following pretreatment with 10 μM STO-609 for 4 h and CaMKKβ siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 6 h. (B,H) The mRNA expression of M2 microglial markers (Arg-1, CD206, and YM1/2) were detected via RT-PCR. (C,I) The mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) were detected via RT-PCR. Pretreatment with 10 μM STO-609 for 4 h and CaMKKβ siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 24 h. (C,G) The release of IL-10 was measured with ELISA. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4 in each group). ## p
    Figure Legend Snippet: CaMKKβ activation is involved in IVX-mediated microglial polarization in BV-2 cells and mouse primary microglia. (D) After treatment with CaMKKβ siRNA for 24 h and then IVX for 2 h in mouse primary microglia, the protein expression of CaMKKβ was measured with Western blotting. (E) After treated with CaMKKβ siRNA for 24 h, mouse primary microglia were exposed to IVX for 1 h. The protein expression of p-AMPK was detected by Western blotting. (F) After treated with CaMKKβ siRNA for 24 h, mouse primary microglia were exposed to IVX for 3 h. The protein expression of PGC-1α was detected by Western blotting. Following pretreatment with 10 μM STO-609 for 4 h and CaMKKβ siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 6 h. (B,H) The mRNA expression of M2 microglial markers (Arg-1, CD206, and YM1/2) were detected via RT-PCR. (C,I) The mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) were detected via RT-PCR. Pretreatment with 10 μM STO-609 for 4 h and CaMKKβ siRNA for 24 h, cells were treated with IVX (200 μg/mL) for 2 h and then stimulated with LPS (100 ng/mL) for 24 h. (C,G) The release of IL-10 was measured with ELISA. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4 in each group). ## p

    Techniques Used: Activation Assay, Expressing, Western Blot, Pyrolysis Gas Chromatography, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    Isovitexin (IVX) inhibited M1 microglial polarization and promoted M2 microglial polarization in LPS-activated BV-2 cells and mouse primary microglia. (D) The purity of mouse primary microglia was detected by Fluorescent immunocytochemistry. BV-2 cells and mouse primary microglia were pretreated with IVX (200 μg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h and 24 h. After 6 h, cells were then harvested and the mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) and M2 microglia markers (Arg-1, CD206, and YM1/2) were detected by RT-PCR. (A,E) IVX inhibited the mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) in LPS-activated BV-2 cells and mouse primary microglia. (B,F) IVX attenuated the decrease of M2 microglial markers (Arg-1, CD206, and YM1/2) in LPS-activated BV-2 cells and mouse primary microglia. After 24 h, cells medium were harvested and the release of IL-10 were investigated by ELISA. (C,G) IVX enhanced the release of IL-10 in LPS-activated BV-2 cells and mouse primary microglia. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4 in each group). # p
    Figure Legend Snippet: Isovitexin (IVX) inhibited M1 microglial polarization and promoted M2 microglial polarization in LPS-activated BV-2 cells and mouse primary microglia. (D) The purity of mouse primary microglia was detected by Fluorescent immunocytochemistry. BV-2 cells and mouse primary microglia were pretreated with IVX (200 μg/mL) for 2 h and then treated with LPS (100 ng/mL) for 6 h and 24 h. After 6 h, cells were then harvested and the mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) and M2 microglia markers (Arg-1, CD206, and YM1/2) were detected by RT-PCR. (A,E) IVX inhibited the mRNA expression of M1 microglial markers (TNF-α, IL-6, IL-1β, iNOS, and COX-2) in LPS-activated BV-2 cells and mouse primary microglia. (B,F) IVX attenuated the decrease of M2 microglial markers (Arg-1, CD206, and YM1/2) in LPS-activated BV-2 cells and mouse primary microglia. After 24 h, cells medium were harvested and the release of IL-10 were investigated by ELISA. (C,G) IVX enhanced the release of IL-10 in LPS-activated BV-2 cells and mouse primary microglia. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4 in each group). # p

    Techniques Used: Immunocytochemistry, Expressing, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    IVX-mediated PGC-1α activation inhibited M1 microglial polarization and promoted M2 microglial polarization in the cerebral cortices of LPS-injected mice. After the open field test, the cerebral cortices of mice were harvested. In LPS-injected mice, to investigate the effect of IVX-mediated PGC-1α activation on microglial polarization, the mRNA and protein expression of M1 microglial markers (TNF-α and iNOS) and M2 microglial markers (Arg-1 and CD206) were tested via RT-PCR and western blotting. (A,B) The mRNA expression of M1 microglial markers (TNF-α and iNOS) were measured via RT-PCR. (C,D) The mRNA expression of M2 microglial markers (Arg-1 and CD206) was measured via RT-PCR. (F–H) The protein expression of M1 microglial markers (TNF-α and iNOS) were measured via western blotting. (I,J) The protein expression of M2 microglial markers (Arg-1 and CD206) was measured via western blotting. (E,K) The gene and protein expression of IL-10 was measured via RT-PCR and western blotting. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4–5 in each group). # p
    Figure Legend Snippet: IVX-mediated PGC-1α activation inhibited M1 microglial polarization and promoted M2 microglial polarization in the cerebral cortices of LPS-injected mice. After the open field test, the cerebral cortices of mice were harvested. In LPS-injected mice, to investigate the effect of IVX-mediated PGC-1α activation on microglial polarization, the mRNA and protein expression of M1 microglial markers (TNF-α and iNOS) and M2 microglial markers (Arg-1 and CD206) were tested via RT-PCR and western blotting. (A,B) The mRNA expression of M1 microglial markers (TNF-α and iNOS) were measured via RT-PCR. (C,D) The mRNA expression of M2 microglial markers (Arg-1 and CD206) was measured via RT-PCR. (F–H) The protein expression of M1 microglial markers (TNF-α and iNOS) were measured via western blotting. (I,J) The protein expression of M2 microglial markers (Arg-1 and CD206) was measured via western blotting. (E,K) The gene and protein expression of IL-10 was measured via RT-PCR and western blotting. The experiments were conducted in triplicate and repeated at least three times. Values are expressed as mean ± SEM ( n = 4–5 in each group). # p

    Techniques Used: Pyrolysis Gas Chromatography, Activation Assay, Injection, Mouse Assay, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot

    20) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    21) Product Images from "Sleep deprivation aggravates brain injury after experimental subarachnoid hemorrhage via TLR4-MyD88 pathway"

    Article Title: Sleep deprivation aggravates brain injury after experimental subarachnoid hemorrhage via TLR4-MyD88 pathway

    Journal: Aging (Albany NY)

    doi: 10.18632/aging.202503

    Sleep deprivation regulates neuroinflammation after SAH. ( A ) Cytochemistry assay shows that sleep deprivation increased the number of Iba-1 positive cells after SAH. ( B ) Western blot shows that sleep deprivation increased the expression of Iba-1 after SAH. ( C – F ) ELISA shows that sleep deprivation increased the levels of IL-1β ( C ) and TNF-α ( D ), but decreased the levels of IL-10 ( E ) and TGF-β1 ( F ) after SAH in rats. The data was represented as means ± SEM. # p
    Figure Legend Snippet: Sleep deprivation regulates neuroinflammation after SAH. ( A ) Cytochemistry assay shows that sleep deprivation increased the number of Iba-1 positive cells after SAH. ( B ) Western blot shows that sleep deprivation increased the expression of Iba-1 after SAH. ( C – F ) ELISA shows that sleep deprivation increased the levels of IL-1β ( C ) and TNF-α ( D ), but decreased the levels of IL-10 ( E ) and TGF-β1 ( F ) after SAH in rats. The data was represented as means ± SEM. # p

    Techniques Used: Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

    Involvement of TLR4-MyD88 pathway in sleep deprivation-induced aggravation of brain injury after SAH. ( A ) Brain water content assay shows that aggravation of brain edema induced by sleep deprivation after SAH was prevented by TAK-242 and ST2825. ( B ) TUNEL staining shows that the increase in apoptosis induced by sleep deprivation after SAH was inhibited by TAK-242 and ST2825. ( C – E ) Western blot ( C ) and quantification ( D , E ) show that the increased expression of C-caspase-3 ( D ) and Iba-1 ( E ) induced by sleep deprivation after SAH was prevented by TAK-242 and ST2825. ( F – I ) ELISA shows that the increased levels of IL-1β ( F ) and TNF-α ( G ) and decreased the levels of IL-10 ( H ) and TGF-β1 ( I ) induced by sleep deprivation after SAH were reversed by TAK-242 and ST2825. ( J ) Neurological score assay shows that aggravation of neurological impairment induced by sleep deprivation after SAH was prevented by TAK-242 and ST2825. The data was represented as means ± SEM. # p
    Figure Legend Snippet: Involvement of TLR4-MyD88 pathway in sleep deprivation-induced aggravation of brain injury after SAH. ( A ) Brain water content assay shows that aggravation of brain edema induced by sleep deprivation after SAH was prevented by TAK-242 and ST2825. ( B ) TUNEL staining shows that the increase in apoptosis induced by sleep deprivation after SAH was inhibited by TAK-242 and ST2825. ( C – E ) Western blot ( C ) and quantification ( D , E ) show that the increased expression of C-caspase-3 ( D ) and Iba-1 ( E ) induced by sleep deprivation after SAH was prevented by TAK-242 and ST2825. ( F – I ) ELISA shows that the increased levels of IL-1β ( F ) and TNF-α ( G ) and decreased the levels of IL-10 ( H ) and TGF-β1 ( I ) induced by sleep deprivation after SAH were reversed by TAK-242 and ST2825. ( J ) Neurological score assay shows that aggravation of neurological impairment induced by sleep deprivation after SAH was prevented by TAK-242 and ST2825. The data was represented as means ± SEM. # p

    Techniques Used: TUNEL Assay, Staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

    22) Product Images from "CFTR protects against vascular inflammation and atherogenesis in apolipoprotein E-deficient mice"

    Article Title: CFTR protects against vascular inflammation and atherogenesis in apolipoprotein E-deficient mice

    Journal: Bioscience Reports

    doi: 10.1042/BSR20170680

    CFTR reduced inflammatory cytokines in aorta and peritoneal macrophages from atherosclerotic mice ( A,B ) RT-PCR analysis for the mRNA expression of MCP-1, TNF-α, IL-1β, and IL-6 (A), and IL-10, Ym1, Mgl2, and Arg1 (B) in aorta from HFD-fed apoE −/− mice treated with Ad-LacZ or Ad-CFTR. ** P
    Figure Legend Snippet: CFTR reduced inflammatory cytokines in aorta and peritoneal macrophages from atherosclerotic mice ( A,B ) RT-PCR analysis for the mRNA expression of MCP-1, TNF-α, IL-1β, and IL-6 (A), and IL-10, Ym1, Mgl2, and Arg1 (B) in aorta from HFD-fed apoE −/− mice treated with Ad-LacZ or Ad-CFTR. ** P

    Techniques Used: Mouse Assay, Reverse Transcription Polymerase Chain Reaction, Expressing

    23) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    24) Product Images from "Protective effect of Chrysanthemum morifolium Ramat. ethanol extract on lipopolysaccharide induced acute lung injury in mice"

    Article Title: Protective effect of Chrysanthemum morifolium Ramat. ethanol extract on lipopolysaccharide induced acute lung injury in mice

    Journal: BMC Complementary Medicine and Therapies

    doi: 10.1186/s12906-020-03017-z

    Effect of CEE on the levels of TGF- β 1 and IL-10 in lung tissue of ALI mice ( n = 18). ## P
    Figure Legend Snippet: Effect of CEE on the levels of TGF- β 1 and IL-10 in lung tissue of ALI mice ( n = 18). ## P

    Techniques Used: Mouse Assay

    25) Product Images from "Unravelling Heterogeneity of Amplified Human Amniotic Fluid Stem Cells Sub-Populations"

    Article Title: Unravelling Heterogeneity of Amplified Human Amniotic Fluid Stem Cells Sub-Populations

    Journal: Cells

    doi: 10.3390/cells10010158

    Analysis of the secretome produced by hAFSC fractions. ( A ) Graph representing ELISA tests for TGFβ, HGF, IDO, IL-10 and IL-6 analysed in condition medium (CM) produced by initial and final eluted cells obtained from 3 donors. The ratio between final and initial CM is shown. T test statistical analysis was performed to evaluate the difference between CM of final cells compared to the one of initial cells. * p value
    Figure Legend Snippet: Analysis of the secretome produced by hAFSC fractions. ( A ) Graph representing ELISA tests for TGFβ, HGF, IDO, IL-10 and IL-6 analysed in condition medium (CM) produced by initial and final eluted cells obtained from 3 donors. The ratio between final and initial CM is shown. T test statistical analysis was performed to evaluate the difference between CM of final cells compared to the one of initial cells. * p value

    Techniques Used: Produced, Enzyme-linked Immunosorbent Assay

    26) Product Images from "Polysaccharides from Hericium erinaceus Fruiting Bodies: Structural Characterization, Immunomodulatory Activity and Mechanism"

    Article Title: Polysaccharides from Hericium erinaceus Fruiting Bodies: Structural Characterization, Immunomodulatory Activity and Mechanism

    Journal: Nutrients

    doi: 10.3390/nu14183721

    Effects of HEP-1 in RAW264.7/Caco-2 cells model. ( A ) IL-6. ( B ) IFN-γ. ( C ) IL-10. ( D ) TNF-α. After the treatment of inhibitors including BAY11-7082, SB203580, SP600126, PD98095 and LY294002, the release of ( E ) NO and ( F ) TNF-α in NF-κB, MAPK and PI3K/Akt signaling pathways were detected. Data are presented as mean ± SD ( n = 3). * p
    Figure Legend Snippet: Effects of HEP-1 in RAW264.7/Caco-2 cells model. ( A ) IL-6. ( B ) IFN-γ. ( C ) IL-10. ( D ) TNF-α. After the treatment of inhibitors including BAY11-7082, SB203580, SP600126, PD98095 and LY294002, the release of ( E ) NO and ( F ) TNF-α in NF-κB, MAPK and PI3K/Akt signaling pathways were detected. Data are presented as mean ± SD ( n = 3). * p

    Techniques Used:

    27) Product Images from "Gut Microbiota Modulates Intestinal Pathological Injury in Schistosoma japonicum-Infected Mice"

    Article Title: Gut Microbiota Modulates Intestinal Pathological Injury in Schistosoma japonicum-Infected Mice

    Journal: Frontiers in Medicine

    doi: 10.3389/fmed.2020.588928

    Transfer of the gut microbiota from normal mice to infected mice regulated intestinal inflammatory cytokine production in infected mice. (A) The levels of IL-4, IL-5, IL-13, IL-10, and TGF-β in the intestine were detected by immunohistochemistry. Cell nuclei were counterstained with haematoxylin. (B) The area of the entire tissue and the positive area were analyzed with Image-Pro Plus 6.0 software. (C) The mRNA of IL-4, IL-5, IL-13, IL-10, and TGF-β in the intestine were detected by Real-time qPCR. * = p
    Figure Legend Snippet: Transfer of the gut microbiota from normal mice to infected mice regulated intestinal inflammatory cytokine production in infected mice. (A) The levels of IL-4, IL-5, IL-13, IL-10, and TGF-β in the intestine were detected by immunohistochemistry. Cell nuclei were counterstained with haematoxylin. (B) The area of the entire tissue and the positive area were analyzed with Image-Pro Plus 6.0 software. (C) The mRNA of IL-4, IL-5, IL-13, IL-10, and TGF-β in the intestine were detected by Real-time qPCR. * = p

    Techniques Used: Mouse Assay, Infection, Immunohistochemistry, Software, Real-time Polymerase Chain Reaction

    Depletion of the gut microbiota regulated intestinal inflammatory cytokine production in infected mice. (A) The levels of IL-4, IL-5, IL-13, IL-10, and TGF-β in the intestine were detected by immunohistochemistry. Cell nuclei were counterstained with haematoxylin. (B) The area of the entire tissue and the positive area were analyzed with Image-Pro Plus 6.0 software. (C) The mRNA of IL-4, IL-5, IL-13, IL-10, and TGF-β in the intestine were detected by Real-time qPCR. * = p
    Figure Legend Snippet: Depletion of the gut microbiota regulated intestinal inflammatory cytokine production in infected mice. (A) The levels of IL-4, IL-5, IL-13, IL-10, and TGF-β in the intestine were detected by immunohistochemistry. Cell nuclei were counterstained with haematoxylin. (B) The area of the entire tissue and the positive area were analyzed with Image-Pro Plus 6.0 software. (C) The mRNA of IL-4, IL-5, IL-13, IL-10, and TGF-β in the intestine were detected by Real-time qPCR. * = p

    Techniques Used: Infection, Mouse Assay, Immunohistochemistry, Software, Real-time Polymerase Chain Reaction

    28) Product Images from "Ac2-26 mitigated acute respiratory distress syndrome rats via formyl peptide receptor pathway"

    Article Title: Ac2-26 mitigated acute respiratory distress syndrome rats via formyl peptide receptor pathway

    Journal: Annals of Medicine

    doi: 10.1080/07853890.2021.1925149

    The effect of Ac2-26 on local and systemic inflammation. The levels of TNF-α, IL-1β, IL-6, and IL-10 in serum and BALF were determined by ELISA. The number of macrophages and neutrophils in BALF were also detected. The TNF-α, IL-1β, IL-6, and IL-10 in serum and BALF, and the macrophages and neutrophils in BALF increased in ARDS rats. The TNF-α, IL-1β, IL-6, macrophages, and neutrophils were all reduced by Ac2-26, and the effect of Ac2-26 was reversed by BOC-2. The level of IL-10 increased after the administration of Ac2-26, and this effect was reversed by BOC-2. The data were expressed as mean ± SD. a p
    Figure Legend Snippet: The effect of Ac2-26 on local and systemic inflammation. The levels of TNF-α, IL-1β, IL-6, and IL-10 in serum and BALF were determined by ELISA. The number of macrophages and neutrophils in BALF were also detected. The TNF-α, IL-1β, IL-6, and IL-10 in serum and BALF, and the macrophages and neutrophils in BALF increased in ARDS rats. The TNF-α, IL-1β, IL-6, macrophages, and neutrophils were all reduced by Ac2-26, and the effect of Ac2-26 was reversed by BOC-2. The level of IL-10 increased after the administration of Ac2-26, and this effect was reversed by BOC-2. The data were expressed as mean ± SD. a p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    29) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    30) Product Images from "Bufei Yishen Formula Restores Th17/Treg Balance and Attenuates Chronic Obstructive Pulmonary Disease via Activation of the Adenosine 2a Receptor"

    Article Title: Bufei Yishen Formula Restores Th17/Treg Balance and Attenuates Chronic Obstructive Pulmonary Disease via Activation of the Adenosine 2a Receptor

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2020.01212

    Effect of Bufei Yishen formula (BYF) on Th17 and Treg cell differentiation. Naïve CD4+ T cells were isolated from spleens of mice, and treated with Th17 differentiation conditions or Treg differentiation conditions in the presence or absence of BYF (60 μg/ml) or KW6002 (0.1 μM) for 3 days. (A) the effect of BYF and KW6002 on cell viability of Naïve CD4+ T cells. (B) The mRNA levels for Foxp3. (C) The mRNA levels IL-10. (D) The protein level of Foxp3. (E) RORγt mRNA; (F) IL-17 mRNA; (G) RORγt protein. *P
    Figure Legend Snippet: Effect of Bufei Yishen formula (BYF) on Th17 and Treg cell differentiation. Naïve CD4+ T cells were isolated from spleens of mice, and treated with Th17 differentiation conditions or Treg differentiation conditions in the presence or absence of BYF (60 μg/ml) or KW6002 (0.1 μM) for 3 days. (A) the effect of BYF and KW6002 on cell viability of Naïve CD4+ T cells. (B) The mRNA levels for Foxp3. (C) The mRNA levels IL-10. (D) The protein level of Foxp3. (E) RORγt mRNA; (F) IL-17 mRNA; (G) RORγt protein. *P

    Techniques Used: Cell Differentiation, Isolation, Mouse Assay

    Effect of cotreatment of Bufei Yishen formula (BYF) and A2aR antagonist on cytokine profiles in chronic obstructive pulmonary disease (COPD) rats. COPD rats were orally administrated with BYF, KW6002 and aminophylline. Cytokine levels of f IL-1β, TNF-α, IL-6, IL-17A, and IL-10 in serum or lung tissues were detected by ELISA. The results were independently replicated. The values are presented as the means ± SEM (n= 6 mice per group). *P
    Figure Legend Snippet: Effect of cotreatment of Bufei Yishen formula (BYF) and A2aR antagonist on cytokine profiles in chronic obstructive pulmonary disease (COPD) rats. COPD rats were orally administrated with BYF, KW6002 and aminophylline. Cytokine levels of f IL-1β, TNF-α, IL-6, IL-17A, and IL-10 in serum or lung tissues were detected by ELISA. The results were independently replicated. The values are presented as the means ± SEM (n= 6 mice per group). *P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Mouse Assay

    31) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    32) Product Images from "Melatonin ameliorates Parkinson’s disease via regulating microglia polarization in a RORα‐dependent pathway"

    Article Title: Melatonin ameliorates Parkinson’s disease via regulating microglia polarization in a RORα‐dependent pathway

    Journal: NPJ Parkinson's Disease

    doi: 10.1038/s41531-022-00352-5

    The deficiency of RORα promoted inflammation. BV2 cells were firstly transfected with siRNA for 48 h to knock down RORα expression. MPP + (50 μM), MLT (50 μM), SR3335 (a synthetic selective inverse agonist of RORα, 10 μM), SR1078 (a synthetic agonist of RORα, 10 μM) were applied alone or combined (MLT, SR3335 and SR1078 were treated half an hour before MPP + ) for 24 h. a ELISA results indicated cell culture medium levels of TNF‐α, IL‐1β and IL‐10. b , c Immunofluorescent staining images of iNOS (green) and ARG-1 (red). Blue indicates nuclei. Scale bars = 50 μm. d RT-qPCR results showed the quantitative analysis of polarization markers iNOS and ARG-1 expressions in different cell groups. Data were average with error bars representing standard deviation. ( n = 3 independent experiments.* P
    Figure Legend Snippet: The deficiency of RORα promoted inflammation. BV2 cells were firstly transfected with siRNA for 48 h to knock down RORα expression. MPP + (50 μM), MLT (50 μM), SR3335 (a synthetic selective inverse agonist of RORα, 10 μM), SR1078 (a synthetic agonist of RORα, 10 μM) were applied alone or combined (MLT, SR3335 and SR1078 were treated half an hour before MPP + ) for 24 h. a ELISA results indicated cell culture medium levels of TNF‐α, IL‐1β and IL‐10. b , c Immunofluorescent staining images of iNOS (green) and ARG-1 (red). Blue indicates nuclei. Scale bars = 50 μm. d RT-qPCR results showed the quantitative analysis of polarization markers iNOS and ARG-1 expressions in different cell groups. Data were average with error bars representing standard deviation. ( n = 3 independent experiments.* P

    Techniques Used: Transfection, Expressing, Enzyme-linked Immunosorbent Assay, Cell Culture, Staining, Quantitative RT-PCR, Standard Deviation

    The level of RORα was reduced in BV2s treated with MPP + . BV2 cells were treated in different concentrations (0, 10, 20, 50 μM) of MPP + for 24 h. a Relative mRNA levels of RORα were measured by RT-qPCR. b , c Immunoblot analysis of RORα. Protein expression levels were normalized to GAPDH. d ELISA assays showed the levels of IL-6, TNF-α, IL-1β, and IL-10 in culture medium. Data were average with error bars representing standard deviation. ( n = 3 independent experiments. * P
    Figure Legend Snippet: The level of RORα was reduced in BV2s treated with MPP + . BV2 cells were treated in different concentrations (0, 10, 20, 50 μM) of MPP + for 24 h. a Relative mRNA levels of RORα were measured by RT-qPCR. b , c Immunoblot analysis of RORα. Protein expression levels were normalized to GAPDH. d ELISA assays showed the levels of IL-6, TNF-α, IL-1β, and IL-10 in culture medium. Data were average with error bars representing standard deviation. ( n = 3 independent experiments. * P

    Techniques Used: Quantitative RT-PCR, Expressing, Enzyme-linked Immunosorbent Assay, Standard Deviation

    MLT increased RORα expression, inhibited pro-inflammatory M1-like microglial polarization and reduced neuroinflammation in vitro. BV2 cells were treated with MPP + (50 μM), MLT (50 μM) or pre-treated with MLT half an hour before MPP + , and then incubated for 24 h. a Relative mRNA levels of RORα in different groups were determined by RT-qPCR. b , c Immunoblot analysis of RORα. Protein levels were normalized to GAPDH. d ELISA results showed the culture medium levels of IL-6, TNF-α, IL-1β, IL-4, and IL-10. e mRNA quantification of pro-inflammatory (M1-like) phenotype markers (CD36, iNOS, TNF-α, IL-1β) in BV2 cells by RT-qPCR. f mRNA quantification of anti-inflammatory (M2-like) phenotype markers (CD206, ARG‐1) in BV2 cells. g mRNA quantification of DAM phenotype markers (TREM2, TLR4) in BV2 cells. Data were average with error bars representing standard deviation. ( n = 3 independent experiments. *, # P
    Figure Legend Snippet: MLT increased RORα expression, inhibited pro-inflammatory M1-like microglial polarization and reduced neuroinflammation in vitro. BV2 cells were treated with MPP + (50 μM), MLT (50 μM) or pre-treated with MLT half an hour before MPP + , and then incubated for 24 h. a Relative mRNA levels of RORα in different groups were determined by RT-qPCR. b , c Immunoblot analysis of RORα. Protein levels were normalized to GAPDH. d ELISA results showed the culture medium levels of IL-6, TNF-α, IL-1β, IL-4, and IL-10. e mRNA quantification of pro-inflammatory (M1-like) phenotype markers (CD36, iNOS, TNF-α, IL-1β) in BV2 cells by RT-qPCR. f mRNA quantification of anti-inflammatory (M2-like) phenotype markers (CD206, ARG‐1) in BV2 cells. g mRNA quantification of DAM phenotype markers (TREM2, TLR4) in BV2 cells. Data were average with error bars representing standard deviation. ( n = 3 independent experiments. *, # P

    Techniques Used: Expressing, In Vitro, Incubation, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Standard Deviation

    Expression of RORα was decreased in MPTP-treated mice and MLT showed an anti-inflammatory effect to attenuate MPTP. The mice were treated with MPTP (25 mg/kg, i.p.) or pre-treated with MLT (20 mg/kg, i.p.) half an hour before MPTP injection for 7 days. The levels of RORα in midbrain tissues were measured a week after the behavioural tests. a Relative mRNA levels of RORα were measured by RT-qPCR. b , c Protein levels of RORα, normalized to GAPDH. d ELISA results indicated the serum levels of TNF‐α, IL‐6, IL‐1β, IL-4 and IL‐10. e Representative immunofluorescent staining images of TH in SN. Blue indicates nuclei. TH were labeled as red. Scale bars = 500 μm. f The number of TH + cells in midbrain (represented as fold of sham). g mRNA quantification of pro-inflammatory (M1-like) phenotype markers (CD36, iNOS, TNF-α, IL-1β) in midbrain tissue by RT-qPCR. h mRNA quantification of anti-inflammatory (M2-like) markers (CD206, ARG‐1) in midbrain tissue. i mRNA quantification of DAM phenotype markers (TREM2, TLR4) in midbrain tissue. Data were average with error bars representing standard deviation. ( n = 5 per group. *, # P
    Figure Legend Snippet: Expression of RORα was decreased in MPTP-treated mice and MLT showed an anti-inflammatory effect to attenuate MPTP. The mice were treated with MPTP (25 mg/kg, i.p.) or pre-treated with MLT (20 mg/kg, i.p.) half an hour before MPTP injection for 7 days. The levels of RORα in midbrain tissues were measured a week after the behavioural tests. a Relative mRNA levels of RORα were measured by RT-qPCR. b , c Protein levels of RORα, normalized to GAPDH. d ELISA results indicated the serum levels of TNF‐α, IL‐6, IL‐1β, IL-4 and IL‐10. e Representative immunofluorescent staining images of TH in SN. Blue indicates nuclei. TH were labeled as red. Scale bars = 500 μm. f The number of TH + cells in midbrain (represented as fold of sham). g mRNA quantification of pro-inflammatory (M1-like) phenotype markers (CD36, iNOS, TNF-α, IL-1β) in midbrain tissue by RT-qPCR. h mRNA quantification of anti-inflammatory (M2-like) markers (CD206, ARG‐1) in midbrain tissue. i mRNA quantification of DAM phenotype markers (TREM2, TLR4) in midbrain tissue. Data were average with error bars representing standard deviation. ( n = 5 per group. *, # P

    Techniques Used: Expressing, Mouse Assay, Injection, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Staining, Labeling, Standard Deviation

    33) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

    34) Product Images from "Butyrate as a bioactive human milk protective component against food allergy, et al. Butyrate as a bioactive human milk protective component against food allergy"

    Article Title: Butyrate as a bioactive human milk protective component against food allergy, et al. Butyrate as a bioactive human milk protective component against food allergy

    Journal: Allergy

    doi: 10.1111/all.14625

    Preventive HM butyrate action against FA in the animal model. A, The experimental design of the food allergy mouse model. Four‐week‐old female C3H/HeJ mice (n = 4 in each group) were used in the FA animal model. Two weeks before first sensitization, oral gavage with 30 mg/kg/d of butyrate was started and continued throughout the study. The mice were sensitized orally on days 0, 7, 14, 21, and 28, with 20 mg of BLG, 1 mg of OVA, or 12 mg of PN mixed with 10 μg cholera toxin (CT) as adjuvant. The control mice receive CT only. On day 35, the mice were challenged by gavage with BLG (50 mg), OVA (5 mg), or PN (36 mg). Anaphylaxis scores and rectal temperatures were assessed for 1 h after challenge, and blood samples were collected to measure mMCP‐1 and sIgE. After 24 h, the mice were killed, and their serum and tissues were collected. Two independent experiments were performed. Oral butyrate treatment significantly reduced anaphylactic score (B), serum MCP‐1 (C) and sIgE levels against BLG (D), OVA (E), and PN (F). Splenocytes from FA‐sensitized mice were stimulated 1 μg/mL of anti‐CD3 (clone 2C11) or 200 μg/mL BLG/OVA/PN and incubated at 37°C for 72 h. Butyrate inhibited IL‐4 (G) and IL‐13 (H) production and stimulated IL‐10 (I) and IFN‐γ (L) production in BLG‐, OVA‐, and PN‐sensitized mice. H 2 O 2 yield (M), SOD (N), and ROS‐induced damage on aconitase activity (O) were measured in hepatic mitochondria. The mitochondrial ROS‐induced dysfunction was proven by the higher mitochondrial H 2 O 2 yield, higher SOD activity, and lower basal/total aconitase ratio observed in all FA‐sensitized animals compared with the control group. Butyrate administration positively modulates the oxidative stress as demonstrated by the lower H 2 O 2 release, the decreased SOD activity, and the reactivation of the aconitase enzyme in all treated groups compared with control animals. Data are representative of at least 2 independent experiments, reported as median with range, and analyzed using the unpaired t test. BLG, mice sensitized with β‐lactoglobulin; CTRL, control mice; OVA, mice sensitized with ovalbumin; PN, mice sensitized with peanut extract. * P
    Figure Legend Snippet: Preventive HM butyrate action against FA in the animal model. A, The experimental design of the food allergy mouse model. Four‐week‐old female C3H/HeJ mice (n = 4 in each group) were used in the FA animal model. Two weeks before first sensitization, oral gavage with 30 mg/kg/d of butyrate was started and continued throughout the study. The mice were sensitized orally on days 0, 7, 14, 21, and 28, with 20 mg of BLG, 1 mg of OVA, or 12 mg of PN mixed with 10 μg cholera toxin (CT) as adjuvant. The control mice receive CT only. On day 35, the mice were challenged by gavage with BLG (50 mg), OVA (5 mg), or PN (36 mg). Anaphylaxis scores and rectal temperatures were assessed for 1 h after challenge, and blood samples were collected to measure mMCP‐1 and sIgE. After 24 h, the mice were killed, and their serum and tissues were collected. Two independent experiments were performed. Oral butyrate treatment significantly reduced anaphylactic score (B), serum MCP‐1 (C) and sIgE levels against BLG (D), OVA (E), and PN (F). Splenocytes from FA‐sensitized mice were stimulated 1 μg/mL of anti‐CD3 (clone 2C11) or 200 μg/mL BLG/OVA/PN and incubated at 37°C for 72 h. Butyrate inhibited IL‐4 (G) and IL‐13 (H) production and stimulated IL‐10 (I) and IFN‐γ (L) production in BLG‐, OVA‐, and PN‐sensitized mice. H 2 O 2 yield (M), SOD (N), and ROS‐induced damage on aconitase activity (O) were measured in hepatic mitochondria. The mitochondrial ROS‐induced dysfunction was proven by the higher mitochondrial H 2 O 2 yield, higher SOD activity, and lower basal/total aconitase ratio observed in all FA‐sensitized animals compared with the control group. Butyrate administration positively modulates the oxidative stress as demonstrated by the lower H 2 O 2 release, the decreased SOD activity, and the reactivation of the aconitase enzyme in all treated groups compared with control animals. Data are representative of at least 2 independent experiments, reported as median with range, and analyzed using the unpaired t test. BLG, mice sensitized with β‐lactoglobulin; CTRL, control mice; OVA, mice sensitized with ovalbumin; PN, mice sensitized with peanut extract. * P

    Techniques Used: Animal Model, Mouse Assay, Incubation, Activity Assay

    Evaluation of direct immunoregulatory action of HM butyrate on human peripheral blood mononuclear cells (PBMCs): Th2/Th1 and IL‐10 response and evaluation of FoxP3 expression. A, PBMCs from children with IgE‐mediated FA were stimulated with butyrate HM median concentration (0.75 mM) or with BLG, OVA, and PN (100 μL/well) in the presence or in the absence of butyrate HM median concentration for 24 h. BLG, OVA, and PN induced a significant increase in IL‐4 (A), IL‐5, and IL‐13 (C) production, but the presence of 0.75 mM butyrate significantly reduced the release of these Th2 cytokines. Butyrate alone or in the presence of specific allergen stimulated, at the same dose, IL‐10 (D) and IFN‐γ (E) production and FoxP3 expression (F), through a demethylation of respective gene (G, H, I) in CD4+ T cells purified from stimulated PBMCs from children with IgE‐mediated FA. (L) Butyrate treatment significantly reduced HDAC activity in a dose‐dependent manner in PBMCs. Data represent the median with range of 2 independent experiments, each performed in triplicate. Data were analyzed using the unpaired t test. BLG, β‐lactoglobulin; NT, untreated cells; OVA, ovalbumin; PN, peanut extracts. * P
    Figure Legend Snippet: Evaluation of direct immunoregulatory action of HM butyrate on human peripheral blood mononuclear cells (PBMCs): Th2/Th1 and IL‐10 response and evaluation of FoxP3 expression. A, PBMCs from children with IgE‐mediated FA were stimulated with butyrate HM median concentration (0.75 mM) or with BLG, OVA, and PN (100 μL/well) in the presence or in the absence of butyrate HM median concentration for 24 h. BLG, OVA, and PN induced a significant increase in IL‐4 (A), IL‐5, and IL‐13 (C) production, but the presence of 0.75 mM butyrate significantly reduced the release of these Th2 cytokines. Butyrate alone or in the presence of specific allergen stimulated, at the same dose, IL‐10 (D) and IFN‐γ (E) production and FoxP3 expression (F), through a demethylation of respective gene (G, H, I) in CD4+ T cells purified from stimulated PBMCs from children with IgE‐mediated FA. (L) Butyrate treatment significantly reduced HDAC activity in a dose‐dependent manner in PBMCs. Data represent the median with range of 2 independent experiments, each performed in triplicate. Data were analyzed using the unpaired t test. BLG, β‐lactoglobulin; NT, untreated cells; OVA, ovalbumin; PN, peanut extracts. * P

    Techniques Used: Expressing, Concentration Assay, Purification, Activity Assay

    Effects of HM butyrate in basal condition on gut barrier and on cytokine response. Four‐week‐old female C3H/HeJ mice were divided into two groups: (1) control mice (n = 4), receiving water as vehicle; (2) treated mice (n = 4), receiving oral butyrate once daily (30 mg/kg of body weight). After 14 d all mice were killed, and intestine, in particular ileum, jejunum, and colon, spleen, and mesenteric lymph nodes (MLN) were removed. A‐E, Oral butyrate treatment elicited a significant reduction in gut permeability, measured by plasma FITC‐dextran quantification, and increase in IL‐22, occludin, ZO‐1, and Muc2 expression. F‐L, Oral butyrate treatment induced a significant reduction in IL‐4, IL‐5, and IL‐13 and a significant increase in IFN‐γ and IL‐10 expression in MLN and spleen. M‐N, CD4+/CD25+/FoxP3+ cell numbers were increased after butyrate treatment in mouse spleen MLN and colon. Data are representative of at least 2 independent experiments, reported as median with range, and analyzed using the unpaired t test. * P
    Figure Legend Snippet: Effects of HM butyrate in basal condition on gut barrier and on cytokine response. Four‐week‐old female C3H/HeJ mice were divided into two groups: (1) control mice (n = 4), receiving water as vehicle; (2) treated mice (n = 4), receiving oral butyrate once daily (30 mg/kg of body weight). After 14 d all mice were killed, and intestine, in particular ileum, jejunum, and colon, spleen, and mesenteric lymph nodes (MLN) were removed. A‐E, Oral butyrate treatment elicited a significant reduction in gut permeability, measured by plasma FITC‐dextran quantification, and increase in IL‐22, occludin, ZO‐1, and Muc2 expression. F‐L, Oral butyrate treatment induced a significant reduction in IL‐4, IL‐5, and IL‐13 and a significant increase in IFN‐γ and IL‐10 expression in MLN and spleen. M‐N, CD4+/CD25+/FoxP3+ cell numbers were increased after butyrate treatment in mouse spleen MLN and colon. Data are representative of at least 2 independent experiments, reported as median with range, and analyzed using the unpaired t test. * P

    Techniques Used: Mouse Assay, Permeability, Expressing

    35) Product Images from "Identification of Active Compounds From Yi Nationality Herbal Formula Wosi Influencing COX-2 and VCAM-1 Signaling"

    Article Title: Identification of Active Compounds From Yi Nationality Herbal Formula Wosi Influencing COX-2 and VCAM-1 Signaling

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2020.568585

    Effect of Wosi and colchicine treatment on inflammatory cytokines in the serum of MSU crystal-induced acute gouty arthritis rats. The serum level of inflammatory cytokines of experimental rats were quantified using ELISA kits as per manufacturer’s instructions. (A) IL-1β, (B) IL-6(B), (C) IL-2, (D) IFN-γ, and (E) IL-10. The values were expressed as mean ± SEM for ten animals. ### p
    Figure Legend Snippet: Effect of Wosi and colchicine treatment on inflammatory cytokines in the serum of MSU crystal-induced acute gouty arthritis rats. The serum level of inflammatory cytokines of experimental rats were quantified using ELISA kits as per manufacturer’s instructions. (A) IL-1β, (B) IL-6(B), (C) IL-2, (D) IFN-γ, and (E) IL-10. The values were expressed as mean ± SEM for ten animals. ### p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    36) Product Images from "Light-induced dynamic RGD pattern for sequential modulation of macrophage phenotypes"

    Article Title: Light-induced dynamic RGD pattern for sequential modulation of macrophage phenotypes

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2021.04.018

    UV-induced dynamic RGD pattern sequentially regulates BMDM phenotypes. a) Fluorescence images of BMDMs stained for iNOS (green), Arg-1 (red), and nuclei (blue) after culture on the dynamic RGD pattern for 48 h with or without UV irradiation. UV irradiation was performed at 24 h. Scale bar represents 100 μm. b) Corresponding statistical analysis of the numbers of iNOS + or Arg-1 + cells. c) Corresponding secreted levels of TNF-α, IL-1β, IL-10, and TGF-β1 determined by ELISAs. All experiments were carried out at least three times independently and analyzed using Origin software (MicroCal, USA). Data are expressed as the mean ± standard deviation. Significant differences were assessed by the two-tailed Student's t-test for two groups or one-way ANOVA for three or more groups using SPSS (SPSS Inc., Chicago, IL, USA). *p
    Figure Legend Snippet: UV-induced dynamic RGD pattern sequentially regulates BMDM phenotypes. a) Fluorescence images of BMDMs stained for iNOS (green), Arg-1 (red), and nuclei (blue) after culture on the dynamic RGD pattern for 48 h with or without UV irradiation. UV irradiation was performed at 24 h. Scale bar represents 100 μm. b) Corresponding statistical analysis of the numbers of iNOS + or Arg-1 + cells. c) Corresponding secreted levels of TNF-α, IL-1β, IL-10, and TGF-β1 determined by ELISAs. All experiments were carried out at least three times independently and analyzed using Origin software (MicroCal, USA). Data are expressed as the mean ± standard deviation. Significant differences were assessed by the two-tailed Student's t-test for two groups or one-way ANOVA for three or more groups using SPSS (SPSS Inc., Chicago, IL, USA). *p

    Techniques Used: Fluorescence, Staining, Irradiation, Software, Standard Deviation, Two Tailed Test

    37) Product Images from "Tolerogenic Effect Elicited by Protein Fraction Derived From Different Formulas for Dietary Treatment of Cow’s Milk Allergy in Human Cells"

    Article Title: Tolerogenic Effect Elicited by Protein Fraction Derived From Different Formulas for Dietary Treatment of Cow’s Milk Allergy in Human Cells

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2020.604075

    Modulation of Th2/Th1 cytokines production in peripheral mononuclear blood cells from infants affected by cow’s milk allergy. Exposing peripheral mononuclear blood cells (PBMCs) collected from six infants affected by IgE- mediated cow’s milk allergy for 5 days with 25 µg/ml β -lactoglobulin (BLG) resulted in a significant increase of all Th2 cytokine production: IL-4 (A) , IL-5 (B) , IL-13 (C) . The protein fractions derived from the study formulas were unable to increase the production of Th2 cytokines. Whereas, only EHCF-derived protein fraction was able to increase IL-10 (D) and IFN- γ (E) production. Each data point represents the single patient response. Horizontal bars represent the means with SD obtained within each group. Data were analyzed using the paired t-test. *p
    Figure Legend Snippet: Modulation of Th2/Th1 cytokines production in peripheral mononuclear blood cells from infants affected by cow’s milk allergy. Exposing peripheral mononuclear blood cells (PBMCs) collected from six infants affected by IgE- mediated cow’s milk allergy for 5 days with 25 µg/ml β -lactoglobulin (BLG) resulted in a significant increase of all Th2 cytokine production: IL-4 (A) , IL-5 (B) , IL-13 (C) . The protein fractions derived from the study formulas were unable to increase the production of Th2 cytokines. Whereas, only EHCF-derived protein fraction was able to increase IL-10 (D) and IFN- γ (E) production. Each data point represents the single patient response. Horizontal bars represent the means with SD obtained within each group. Data were analyzed using the paired t-test. *p

    Techniques Used: Derivative Assay

    38) Product Images from "Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway"

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    Journal: Open Medicine

    doi: 10.1515/med-2021-0287

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Figure Legend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Techniques Used: Expressing

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    Boster Bio il 10
    P-A regulates expression of IL-6, <t>IL-10,</t> and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P
    Il 10, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Effects of VitD 3 on intestinal permeability and inflammatory cytokine secretion in serum of mice. (a) DAO activity in serum. (b) D-LA concentration in serum. (c) TNF- α concentration in serum. (d) IL-1 β concentration in serum. (e) IL-6 concentration in serum. (f) IL-10 concentration in serum. All data were presented as mean ± SEM ( n = 10). ∗ P

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Vitamin D3 Protects Mice from Diquat-Induced Oxidative Stress through the NF-κB/Nrf2/HO-1 Signaling Pathway

    doi: 10.1155/2021/6776956

    Figure Lengend Snippet: Effects of VitD 3 on intestinal permeability and inflammatory cytokine secretion in serum of mice. (a) DAO activity in serum. (b) D-LA concentration in serum. (c) TNF- α concentration in serum. (d) IL-1 β concentration in serum. (e) IL-6 concentration in serum. (f) IL-10 concentration in serum. All data were presented as mean ± SEM ( n = 10). ∗ P

    Article Snippet: The kits to detect the concentration of TNF-α (Catalog number EK0527), IL-1β (Catalog number EK0394), IL-6 (Catalog number EK0411), and IL-10 (Catalog number EK0417) in serum were purchased from Boster (Wuhan, China).

    Techniques: Permeability, Mouse Assay, Activity Assay, Concentration Assay

    P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Journal: Open Medicine

    Article Title: Novel H2S donor proglumide-ADT-OH protects HUVECs from ox-LDL-induced injury through NF-κB and JAK/SATA pathway

    doi: 10.1515/med-2021-0287

    Figure Lengend Snippet: P-A regulates expression of IL-6, IL-10, and TNF-α through NF-кB and JAK/SATA pathways. (a) The expression of p-NF-кB p65 protein in HUVEC damage model. (1) cell control; (2) model; (3) NaHS; (4) P-A; (5) PDTC + NaHS; (6) PDTC + P-A. * P

    Article Snippet: P-A and proglumide can significantly increase the secretion of IL-10 in the HUVEC damage model.

    Techniques: Expressing