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nmol l tumor necrosis factor  (R&D Systems)


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    R&D Systems nmol l tumor necrosis factor
    Nmol L Tumor Necrosis Factor, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 1752 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tnf%CE%B1/Recombinant+Human+TNF-alpha+Protein/pmc13054578-103-43-49
    Average 97 stars, based on 1752 article reviews
    nmol l tumor necrosis factor - by Bioz Stars, 2026-10
    97/100 stars

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    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Cold exposure increases aortic dissection risk through extracellular cold inducible RNA binding protein and toll like receptor 4 signaling.
    Article Snippet: .. Mouse serum was collected and analyzed by using a CIRP ELISA kit (MyBioSource, MBS7252333), IL-6 (BioLegend, 431307), and TNFα (R&D Systems, MTA00B) according to the manufacturer’s instructions. ..

    Article Title: Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth.
    Article Snippet: .. We used a commercial solidphase ELISA kit protocol to measure IL-1β (Invitrogen, BMS224-2), TNFα (R&D Systems, DY210-05), IL-6 (R&D Systems, DY206-05), IL-8 (R&D Systems, DY208-05), IL-4 (R&D Systems, DY204-05), IL-10 (R&D Systems, DY217B-05), IL-13 (R&D Systems, DY213-05), CCL5 (R&D Systems, DY278-05), CCL17 (R&D Systems, DY364-05), and CCL20 (R&D Systems, DY360-05). .. In vitro in-direct co-culture assay iMac and cancer cell lines were co-cultured using a non-contact co-culture transwell system with 3.0 μm pore polyester membrane inserts (Corning, USA).

    Article Title: Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth
    Article Snippet: .. We used a commercial solid-phase ELISA kit protocol to measure IL-1β (Invitrogen, BMS224-2), TNFα (R&D Systems, DY210-05), IL-6 (R&D Systems, DY206-05), IL-8 (R&D Systems, DY208-05), IL-4 (R&D Systems, DY204-05), IL-10 (R&D Systems, DY217B-05), IL-13 (R&D Systems, DY213-05), CCL5 (R&D Systems, DY278-05), CCL17 (R&D Systems, DY364-05), and CCL20 (R&D Systems, DY360-05). .. iMac and cancer cell lines were co-cultured using a non-contact co-culture transwell system with 3.0 μm pore polyester membrane inserts (Corning, USA).

    Article Title: Poldip2 deficiency attenuates lung disease severity in a mouse model of COVID-19
    Article Snippet: .. Specific mouse sandwich enzyme-linked immunosorbent assays (ELISA) were carried out using kits from R&D Systems: TNFα (MHSTA50), IL-1B/IL-1F2 (MHSLB00), IL-6 (M6000B-1), MCP1/CCL2 (MJE00B), CXCL1/KC (MKC00B-1), IFN-γ (MIF00–1). ..

    RNA Extraction:

    Article Title: Comparative analysis of pathways induced by TMAO and TNF-α in human microvascular endothelial cells.
    Article Snippet: Briefly, HMEC-1 were conditioned at 37°C with 5% CO2 in basal media (MCDB131, Sigma-Aldrich, Saint-Louis, MO, USA) sstupplemented with 20% fetal bovine serum (FBS), 10 ng/mL recombinant human epidermal growth factor, 1% penicillin-streptomycin, and 10 mM L-glutamic acid. .. The cells were treated with 50 μM TMAO (317594, Sigma-Aldrich) or 1 ng/mL TNFα (210-TA, R&D systems, Minneapolis, MN, USA) in serum-starved media (2% FBS) for 48 h. After 48 h, they were harvested and subjected to RNA extraction for sequencing, followed by RT-qPCR validation. ..

    Sequencing:

    Article Title: Comparative analysis of pathways induced by TMAO and TNF-α in human microvascular endothelial cells.
    Article Snippet: Briefly, HMEC-1 were conditioned at 37°C with 5% CO2 in basal media (MCDB131, Sigma-Aldrich, Saint-Louis, MO, USA) sstupplemented with 20% fetal bovine serum (FBS), 10 ng/mL recombinant human epidermal growth factor, 1% penicillin-streptomycin, and 10 mM L-glutamic acid. .. The cells were treated with 50 μM TMAO (317594, Sigma-Aldrich) or 1 ng/mL TNFα (210-TA, R&D systems, Minneapolis, MN, USA) in serum-starved media (2% FBS) for 48 h. After 48 h, they were harvested and subjected to RNA extraction for sequencing, followed by RT-qPCR validation. ..

    Article Title: From bats to humans: uncovering ISG15 as a new resistance factor in type 1 diabetes
    Article Snippet: Human islet microtissues (hIsMTs) (InSphero, MT-04-002-01-60) were generated after dispersion and reaggregation of primary human islets from a single donor (UNOS ID #ALIR128; male; 41y.o. .. ; Hispanic; BMI 27.77; positive serologies: CMV IgG, EBV IgG; HbA1c: 5.3%; cause of death: head trauma). hIsMTs were transduced with AAVs encoding specific shRNA targeting ISG15 (siISG15 #1 sequence) from Vector Biolabs during aggregation for 5 days in Akura hanging drop plates (InSphero, CS-PF24) and then released into Akura 96-well plates (InSphero, CS-09-001-00). hIsMTs were cultured in standard culture medium (InSphero, CS-07-005-01) or standard culture medium containing cytokines: TNFα (25 ng/mL, R&D Systems, 10291-TA-050); IL1β (5 ng/mL, Sigma, H6291-10UG); IFNγ (25 ng/mL, R&D Systems, 10067-IF-100) and IFNα (10 ng/mL, Peprotech, 300-02AA) starting at day 9 after reaggregation, for 6 days. ..

    Quantitative RT-PCR:

    Article Title: Comparative analysis of pathways induced by TMAO and TNF-α in human microvascular endothelial cells.
    Article Snippet: Briefly, HMEC-1 were conditioned at 37°C with 5% CO2 in basal media (MCDB131, Sigma-Aldrich, Saint-Louis, MO, USA) sstupplemented with 20% fetal bovine serum (FBS), 10 ng/mL recombinant human epidermal growth factor, 1% penicillin-streptomycin, and 10 mM L-glutamic acid. .. The cells were treated with 50 μM TMAO (317594, Sigma-Aldrich) or 1 ng/mL TNFα (210-TA, R&D systems, Minneapolis, MN, USA) in serum-starved media (2% FBS) for 48 h. After 48 h, they were harvested and subjected to RNA extraction for sequencing, followed by RT-qPCR validation. ..

    Biomarker Discovery:

    Article Title: Comparative analysis of pathways induced by TMAO and TNF-α in human microvascular endothelial cells.
    Article Snippet: Briefly, HMEC-1 were conditioned at 37°C with 5% CO2 in basal media (MCDB131, Sigma-Aldrich, Saint-Louis, MO, USA) sstupplemented with 20% fetal bovine serum (FBS), 10 ng/mL recombinant human epidermal growth factor, 1% penicillin-streptomycin, and 10 mM L-glutamic acid. .. The cells were treated with 50 μM TMAO (317594, Sigma-Aldrich) or 1 ng/mL TNFα (210-TA, R&D systems, Minneapolis, MN, USA) in serum-starved media (2% FBS) for 48 h. After 48 h, they were harvested and subjected to RNA extraction for sequencing, followed by RT-qPCR validation. ..

    other:

    Article Title: Metabolic and behavioural maladaptations have a rapid onset following short-term obesogenic diet withdrawal in male wistar rats
    Article Snippet: The concentrations of IL6 (#DY506, R&D Systems, US), IL10 (#DY522, R&D Systems, US), IL1β (#DY501, R&D Systems, US), and TNFα (#DY510, R&D Systems, US) were evaluated in the supernatant following the manufacturer’s instructions.

    Transduction:

    Article Title: From bats to humans: uncovering ISG15 as a new resistance factor in type 1 diabetes
    Article Snippet: Human islet microtissues (hIsMTs) (InSphero, MT-04-002-01-60) were generated after dispersion and reaggregation of primary human islets from a single donor (UNOS ID #ALIR128; male; 41y.o. .. ; Hispanic; BMI 27.77; positive serologies: CMV IgG, EBV IgG; HbA1c: 5.3%; cause of death: head trauma). hIsMTs were transduced with AAVs encoding specific shRNA targeting ISG15 (siISG15 #1 sequence) from Vector Biolabs during aggregation for 5 days in Akura hanging drop plates (InSphero, CS-PF24) and then released into Akura 96-well plates (InSphero, CS-09-001-00). hIsMTs were cultured in standard culture medium (InSphero, CS-07-005-01) or standard culture medium containing cytokines: TNFα (25 ng/mL, R&D Systems, 10291-TA-050); IL1β (5 ng/mL, Sigma, H6291-10UG); IFNγ (25 ng/mL, R&D Systems, 10067-IF-100) and IFNα (10 ng/mL, Peprotech, 300-02AA) starting at day 9 after reaggregation, for 6 days. ..

    shRNA:

    Article Title: From bats to humans: uncovering ISG15 as a new resistance factor in type 1 diabetes
    Article Snippet: Human islet microtissues (hIsMTs) (InSphero, MT-04-002-01-60) were generated after dispersion and reaggregation of primary human islets from a single donor (UNOS ID #ALIR128; male; 41y.o. .. ; Hispanic; BMI 27.77; positive serologies: CMV IgG, EBV IgG; HbA1c: 5.3%; cause of death: head trauma). hIsMTs were transduced with AAVs encoding specific shRNA targeting ISG15 (siISG15 #1 sequence) from Vector Biolabs during aggregation for 5 days in Akura hanging drop plates (InSphero, CS-PF24) and then released into Akura 96-well plates (InSphero, CS-09-001-00). hIsMTs were cultured in standard culture medium (InSphero, CS-07-005-01) or standard culture medium containing cytokines: TNFα (25 ng/mL, R&D Systems, 10291-TA-050); IL1β (5 ng/mL, Sigma, H6291-10UG); IFNγ (25 ng/mL, R&D Systems, 10067-IF-100) and IFNα (10 ng/mL, Peprotech, 300-02AA) starting at day 9 after reaggregation, for 6 days. ..

    Cell Culture:

    Article Title: From bats to humans: uncovering ISG15 as a new resistance factor in type 1 diabetes
    Article Snippet: Human islet microtissues (hIsMTs) (InSphero, MT-04-002-01-60) were generated after dispersion and reaggregation of primary human islets from a single donor (UNOS ID #ALIR128; male; 41y.o. .. ; Hispanic; BMI 27.77; positive serologies: CMV IgG, EBV IgG; HbA1c: 5.3%; cause of death: head trauma). hIsMTs were transduced with AAVs encoding specific shRNA targeting ISG15 (siISG15 #1 sequence) from Vector Biolabs during aggregation for 5 days in Akura hanging drop plates (InSphero, CS-PF24) and then released into Akura 96-well plates (InSphero, CS-09-001-00). hIsMTs were cultured in standard culture medium (InSphero, CS-07-005-01) or standard culture medium containing cytokines: TNFα (25 ng/mL, R&D Systems, 10291-TA-050); IL1β (5 ng/mL, Sigma, H6291-10UG); IFNγ (25 ng/mL, R&D Systems, 10067-IF-100) and IFNα (10 ng/mL, Peprotech, 300-02AA) starting at day 9 after reaggregation, for 6 days. ..

    Dot Blot:

    Article Title: Immunomodulatory effects of short-chain fatty acids and immune-supporting nutrients on slice cultures of head and neck tumors
    Article Snippet: .. IL-1β (1:1000;#12703S, Cell signalling), IL-6 (1:500, # MAB206, RnD systems, Minneapolis, USA), IFN- γ (1:500, #ab231036, Abcam), Granzyme B (GrB; 1:200, #3002-MSM4-P1, Invitrogen, Massachusetts, USA) and TNFα (1:500, #MAB610, RnD systems) levels were assessed by the aforementioned antibodies and dilutions using a dot blot approach. .. Circles were lightly drawn with a pencil on Amersham Protran 0.2 μm nitrocellulose membranes (#10600001, GE Healthcare, UK) to mark spots for each supernatant.



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    Image Search Results


    In vivo immunomodulatory effects of different modified surfaces in a DM model. (A) Schematic representation of the animal modeling and experimental treatment workflow. (B, C) hematoxylin and eosin staining of the peri-implant tissues in the femurs of DM rats 1 week after implantation, accompanied by quantitative analysis of the fibrous capsule thickness (scale bar = 100 μm, n = 5). (D–G) Immunofluorescence staining evaluating the polarization state of macrophages surrounding the implants (green: macrophage marker cluster of differentiation (CD) 68; red: M1 marker CD86 and M2 marker CD206; blue: nuclei), along with corresponding quantitative analysis of the fluorescence signals (scale bar = 100 μm, n = 5). (H–K) Immunohistochemical staining assessing the expression of the pro-inflammatory marker tumor necrosis factor-α and the anti-inflammatory marker interleukin-10 in the peri-implant area, with quantitative results of the positive staining areas (scale bar = 100 μm, n = 5). Data are expressed as the mean ± standard deviation, with statistical analysis performed using one-way ANOVA and Tukey's post-hoc test. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicate statistical significance.

    Journal: Bioactive Materials

    Article Title: Integrated apoptotic extracellular vesicle-recruitment peptide coating reprograms the diabetic bone microenvironment and orchestrates enhanced implant osseointegration

    doi: 10.1016/j.bioactmat.2026.05.059

    Figure Lengend Snippet: In vivo immunomodulatory effects of different modified surfaces in a DM model. (A) Schematic representation of the animal modeling and experimental treatment workflow. (B, C) hematoxylin and eosin staining of the peri-implant tissues in the femurs of DM rats 1 week after implantation, accompanied by quantitative analysis of the fibrous capsule thickness (scale bar = 100 μm, n = 5). (D–G) Immunofluorescence staining evaluating the polarization state of macrophages surrounding the implants (green: macrophage marker cluster of differentiation (CD) 68; red: M1 marker CD86 and M2 marker CD206; blue: nuclei), along with corresponding quantitative analysis of the fluorescence signals (scale bar = 100 μm, n = 5). (H–K) Immunohistochemical staining assessing the expression of the pro-inflammatory marker tumor necrosis factor-α and the anti-inflammatory marker interleukin-10 in the peri-implant area, with quantitative results of the positive staining areas (scale bar = 100 μm, n = 5). Data are expressed as the mean ± standard deviation, with statistical analysis performed using one-way ANOVA and Tukey's post-hoc test. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicate statistical significance.

    Article Snippet: For IHC analysis, sections underwent heat-induced antigen retrieval and blocking prior to incubation with antibodies against TNF-α (GB11188, Servicebio, China), IL-10 (GB11534, Servicebio, China), and VEGF (GB15165, Servicebio, China) to identify differences in local inflammatory and angiogenic profiles.

    Techniques: In Vivo, Modification, Staining, Immunofluorescence, Marker, Fluorescence, Immunohistochemical staining, Expressing, Standard Deviation

    SUR1 interacted with PARP1 to suppress DNA damage repair and induce apoptosis of bronchial epithelial cells (A) Co-immunoprecipitation and western blot analyses of HEK293T cells transfected with FLAG-SUR1 plasmids (left) or human bronchial epithlial (HBE) cells (right). (B) Immunofluorescence staining of HBE cells. Scale bars, 25 μm. (C) Homologous recombination reporter assay in U2OS-DRGFP cells transfected with SUR1 siRNA, followed by flow cytometry analysis. (D) Western blot analysis of HBE cells transfected with SUR1 siRNAs with or without 20 ng/mL TNF-α or 50 μg/mL LPS treatment for 1 h. (E) ROS levels in HBE cells with SUR1 knockdown, treated with or without TNF-α 20 ng/mL for 3 h. (F) Apoptosis assay by flow cytometry in HBE cells transfected with SUR1 siRNAs and treated with TNF-α. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Co-localization in (B) was assessed using Pearson’s correlation coefficient. Data in (C–F) were analyzed using two-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

    Journal: iScience

    Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

    doi: 10.1016/j.isci.2026.117627

    Figure Lengend Snippet: SUR1 interacted with PARP1 to suppress DNA damage repair and induce apoptosis of bronchial epithelial cells (A) Co-immunoprecipitation and western blot analyses of HEK293T cells transfected with FLAG-SUR1 plasmids (left) or human bronchial epithlial (HBE) cells (right). (B) Immunofluorescence staining of HBE cells. Scale bars, 25 μm. (C) Homologous recombination reporter assay in U2OS-DRGFP cells transfected with SUR1 siRNA, followed by flow cytometry analysis. (D) Western blot analysis of HBE cells transfected with SUR1 siRNAs with or without 20 ng/mL TNF-α or 50 μg/mL LPS treatment for 1 h. (E) ROS levels in HBE cells with SUR1 knockdown, treated with or without TNF-α 20 ng/mL for 3 h. (F) Apoptosis assay by flow cytometry in HBE cells transfected with SUR1 siRNAs and treated with TNF-α. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Co-localization in (B) was assessed using Pearson’s correlation coefficient. Data in (C–F) were analyzed using two-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

    Article Snippet: Recombinant human TNF-α protein , ABclonal Biotechnology , Cat# RP00001.

    Techniques: Co-Immunoprecipitation Assay, Western Blot, Transfection, Immunofluorescence, Staining, Homologous Recombination, Reporter Assay, Flow Cytometry, Analysis, Knockdown, Apoptosis Assay

    Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS production, caspase-3 activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

    Journal: iScience

    Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

    doi: 10.1016/j.isci.2026.117627

    Figure Lengend Snippet: Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS production, caspase-3 activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

    Article Snippet: Recombinant human TNF-α protein , ABclonal Biotechnology , Cat# RP00001.

    Techniques: RNA Sequencing, Analysis, Control, Quantitative RT-PCR, Co-Immunoprecipitation Assay, Transfection, Fractionation, Western Blot, Activity Assay, Caspase-3 Activity Assay, Flow Cytometry

    Schematic illustration of the role of SUR1 in ALI and the protective mechanism of glibenclamide TNF-α binds to its receptor (TNFR), activating the NF-κB pathway and promoting inflammation through increased transcription of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). In parallel, TNF-α induces mitochondrial dysfunction and ROS production, leading to DNA strand breaks. In response to DNA damage, nuclear PARP1 is activated to recruit DNA repair enzymes, promoting cell survival. Left, SUR1 interacts with and sequesters PARP1, impairing DNA damage repair. Accumulated DNA damage amplifies ROS production and NF-κB activation, which in turn further increases the transcription of inflammatory cytokines. This creates a positive feedback loop that promotes epithelial cell apoptosis and inflammation, contributing to ALI progression. Right, glibenclamide binds to SUR1 and disrupts the SUR1-PARP1 interaction, releasing PARP1 to restore DNA damage repair. This intervention breaks the pathological feedback loop by reducing ROS production, NF-κB activation, and inflammatory cytokine expression, thereby suppressing apoptosis and inflammation in epithelial cells and ultimately protecting against ALI.

    Journal: iScience

    Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

    doi: 10.1016/j.isci.2026.117627

    Figure Lengend Snippet: Schematic illustration of the role of SUR1 in ALI and the protective mechanism of glibenclamide TNF-α binds to its receptor (TNFR), activating the NF-κB pathway and promoting inflammation through increased transcription of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). In parallel, TNF-α induces mitochondrial dysfunction and ROS production, leading to DNA strand breaks. In response to DNA damage, nuclear PARP1 is activated to recruit DNA repair enzymes, promoting cell survival. Left, SUR1 interacts with and sequesters PARP1, impairing DNA damage repair. Accumulated DNA damage amplifies ROS production and NF-κB activation, which in turn further increases the transcription of inflammatory cytokines. This creates a positive feedback loop that promotes epithelial cell apoptosis and inflammation, contributing to ALI progression. Right, glibenclamide binds to SUR1 and disrupts the SUR1-PARP1 interaction, releasing PARP1 to restore DNA damage repair. This intervention breaks the pathological feedback loop by reducing ROS production, NF-κB activation, and inflammatory cytokine expression, thereby suppressing apoptosis and inflammation in epithelial cells and ultimately protecting against ALI.

    Article Snippet: Recombinant human TNF-α protein , ABclonal Biotechnology , Cat# RP00001.

    Techniques: Activation Assay, Expressing

    Journal: iScience

    Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

    doi: 10.1016/j.isci.2026.117627

    Figure Lengend Snippet:

    Article Snippet: Recombinant human TNF-α protein , ABclonal Biotechnology , Cat# RP00001.

    Techniques: Cell-Signaling, Recombinant, Transfection, Caspase-3 Activity Assay, Protein Extraction, Knock-Out, Sequencing, Control, Plasmid Preparation, Software, Analysis

    CRELNVs mitigated memory impairment in the hippocampus of SAE mice. (A) Schematic of the experimental procedure used to probe the effect of CRELNVs on memory impairment in the hippocampi of sepsis‐associated encephalopathy (SAE) mice. (B) Center times in open field test, n = 10. (C) Object discrimination times in novel‐object recognition test, n = 10. (D) Spontaneous alternation rates in Y‐Maze, n = 10. (E) Hematoxylin and eosin, Nissl, and TUNEL staining images. (F) Nissl staining quantitative analysis in CA3 region, n = 6. (G) TUNEL staining quantitative analysis in DG region, n = 6. (H) Interleukin‐1β (IL‐1β), (I) tumor necrosis factor‐α (TNF‐α), (J) interleukin‐6 (IL‐6), and (K) interleukin‐10 (IL‐10) levels in the hippocampi of SAE mice, n = 6. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. lipopolysaccharide (LPS) group.

    Journal: Advanced Science

    Article Title: Chrysanthemum Morifolium– Derived Nanovesicles Reduce Lactate‐Associated Histone Lactylation and Modulate Microglia‐Mediated Neuroinflammation in Sepsis‐Associated Encephalopathy

    doi: 10.1002/advs.78330

    Figure Lengend Snippet: CRELNVs mitigated memory impairment in the hippocampus of SAE mice. (A) Schematic of the experimental procedure used to probe the effect of CRELNVs on memory impairment in the hippocampi of sepsis‐associated encephalopathy (SAE) mice. (B) Center times in open field test, n = 10. (C) Object discrimination times in novel‐object recognition test, n = 10. (D) Spontaneous alternation rates in Y‐Maze, n = 10. (E) Hematoxylin and eosin, Nissl, and TUNEL staining images. (F) Nissl staining quantitative analysis in CA3 region, n = 6. (G) TUNEL staining quantitative analysis in DG region, n = 6. (H) Interleukin‐1β (IL‐1β), (I) tumor necrosis factor‐α (TNF‐α), (J) interleukin‐6 (IL‐6), and (K) interleukin‐10 (IL‐10) levels in the hippocampi of SAE mice, n = 6. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. lipopolysaccharide (LPS) group.

    Article Snippet: IL‐1β (Cat. No. KE10003), IL‐6 (Cat. No. KE10007), TNF‐α (Cat. No. KE10002), and interleukin‐10 (IL‐10; Cat. No. KE1008) Enzyme‐linked immunosorbent assay (ELISA) kits were procured from Proteintech Group (Wuhan, China).

    Techniques: TUNEL Assay, Staining, Analysis, Control

    CRELNVs influence microglial homeostasis in the hippocampus of SAE mice. (A) Representative images of immunofluorescence staining for Iba‐1in the hippocampi of SAE mice. (B) Number of Iba‐1 + cells, (C) number of total branch points/cell, and (D) total branch length for panel A, n = 6. (E) IL‐1β, (F) TNF‐α, (G) IL‐6, and (H) IL‐10 mRNA expression in the hippocampi of SAE mice determined using the quantitative polymerase chain reaction (qPCR), n = 3. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. LPS group).

    Journal: Advanced Science

    Article Title: Chrysanthemum Morifolium– Derived Nanovesicles Reduce Lactate‐Associated Histone Lactylation and Modulate Microglia‐Mediated Neuroinflammation in Sepsis‐Associated Encephalopathy

    doi: 10.1002/advs.78330

    Figure Lengend Snippet: CRELNVs influence microglial homeostasis in the hippocampus of SAE mice. (A) Representative images of immunofluorescence staining for Iba‐1in the hippocampi of SAE mice. (B) Number of Iba‐1 + cells, (C) number of total branch points/cell, and (D) total branch length for panel A, n = 6. (E) IL‐1β, (F) TNF‐α, (G) IL‐6, and (H) IL‐10 mRNA expression in the hippocampi of SAE mice determined using the quantitative polymerase chain reaction (qPCR), n = 3. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. LPS group).

    Article Snippet: IL‐1β (Cat. No. KE10003), IL‐6 (Cat. No. KE10007), TNF‐α (Cat. No. KE10002), and interleukin‐10 (IL‐10; Cat. No. KE1008) Enzyme‐linked immunosorbent assay (ELISA) kits were procured from Proteintech Group (Wuhan, China).

    Techniques: Immunofluorescence, Staining, Expressing, Real-time Polymerase Chain Reaction, Control

    The neuro‐protection and Anti‐inflammation activities of CRELNVs in vitro. (A) Protective effect of CRELNVs on SH‐SY5Y cells in an inflammatory environment determined using the CCK8 assay, n = 4. (B) Microplate reader–detected NO contents in BV2 cell supernatants, n = 3. (C) IL‐1β, (D) IL‐6, (E) TNF‐α, and (F) IL‐10 levels in BV2 cell supernatants, n = 3. (G) Representative fluorescence microscopy images acquired to evaluate reactive oxygen species (ROS) content. (H, I) Flow cytometry peaks and ROS contents derived therefrom, n = 3. (J, K) Western blot analysis: NLRP3 levels in BV2 cells, n = 3. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. LPS group.

    Journal: Advanced Science

    Article Title: Chrysanthemum Morifolium– Derived Nanovesicles Reduce Lactate‐Associated Histone Lactylation and Modulate Microglia‐Mediated Neuroinflammation in Sepsis‐Associated Encephalopathy

    doi: 10.1002/advs.78330

    Figure Lengend Snippet: The neuro‐protection and Anti‐inflammation activities of CRELNVs in vitro. (A) Protective effect of CRELNVs on SH‐SY5Y cells in an inflammatory environment determined using the CCK8 assay, n = 4. (B) Microplate reader–detected NO contents in BV2 cell supernatants, n = 3. (C) IL‐1β, (D) IL‐6, (E) TNF‐α, and (F) IL‐10 levels in BV2 cell supernatants, n = 3. (G) Representative fluorescence microscopy images acquired to evaluate reactive oxygen species (ROS) content. (H, I) Flow cytometry peaks and ROS contents derived therefrom, n = 3. (J, K) Western blot analysis: NLRP3 levels in BV2 cells, n = 3. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. LPS group.

    Article Snippet: IL‐1β (Cat. No. KE10003), IL‐6 (Cat. No. KE10007), TNF‐α (Cat. No. KE10002), and interleukin‐10 (IL‐10; Cat. No. KE1008) Enzyme‐linked immunosorbent assay (ELISA) kits were procured from Proteintech Group (Wuhan, China).

    Techniques: In Vitro, CCK-8 Assay, Fluorescence, Microscopy, Flow Cytometry, Derivative Assay, Western Blot, Analysis, Control

    Plasma interleukin‐6 (IL‐6) concentrations at Days 1, 3, and 7. (a–c) Plasma IL‐6 concentrations at Days 1, 3, and 7, respectively. Plasma IL‐6 concentrations were measured by enzyme‐linked immunosorbent assay at Days 1, 3, and 7. Data are shown as box‐and‐whisker plots with individual data points ( n = 8 per group). Statistical analyses were performed separately at each time point using the Kruskal–Wallis test followed by the Steel–Dwass post hoc test. * p < 0.05, ** p < 0.01. LPS, lipopolysaccharide; Sal, saline; TZD, trazodone.

    Journal: PCN Reports: Psychiatry and Clinical Neurosciences

    Article Title: Acute trazodone treatment ameliorates behavioral abnormalities and improves subsequent short‐term memory in a lipopolysaccharide‐induced mouse model of acute brain dysfunction

    doi: 10.1002/pcn5.70426

    Figure Lengend Snippet: Plasma interleukin‐6 (IL‐6) concentrations at Days 1, 3, and 7. (a–c) Plasma IL‐6 concentrations at Days 1, 3, and 7, respectively. Plasma IL‐6 concentrations were measured by enzyme‐linked immunosorbent assay at Days 1, 3, and 7. Data are shown as box‐and‐whisker plots with individual data points ( n = 8 per group). Statistical analyses were performed separately at each time point using the Kruskal–Wallis test followed by the Steel–Dwass post hoc test. * p < 0.05, ** p < 0.01. LPS, lipopolysaccharide; Sal, saline; TZD, trazodone.

    Article Snippet: Plasma interleukin‐6 (IL‐6) and tumor necrosis factor‐alpha (TNF‐α) concentrations were measured using commercial ELISA kits according to the manufacturers' instructions (Mouse IL‐6 ELISA Kit, KE10007; Mouse TNF‐α ELISA Kit, KE10002; Proteintech Group, Inc.).

    Techniques: Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Whisker Assay, Saline