rat il 1β elisa kit  (Boster Bio)


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    Boster Bio rat il 1β elisa kit
    P2X7R of microglia in spinal cord-mediated neuroinflammation after spinal cord injury. ( A ) <t>ELISA</t> showed that, compared to the sham group, the expression of <t>IL-1β</t> and IL-18 in the spinal cord were significantly increased after spinal cord injury (** P
    Rat Il 1β Elisa Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "P2X7 Receptor (P2X7R) of Microglia Mediates Neuroinflammation by Regulating (NOD)-Like Receptor Protein 3 (NLRP3) Inflammasome-Dependent Inflammation After Spinal Cord Injury"

    Article Title: P2X7 Receptor (P2X7R) of Microglia Mediates Neuroinflammation by Regulating (NOD)-Like Receptor Protein 3 (NLRP3) Inflammasome-Dependent Inflammation After Spinal Cord Injury

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    doi: 10.12659/MSM.925491

    P2X7R of microglia in spinal cord-mediated neuroinflammation after spinal cord injury. ( A ) ELISA showed that, compared to the sham group, the expression of IL-1β and IL-18 in the spinal cord were significantly increased after spinal cord injury (** P
    Figure Legend Snippet: P2X7R of microglia in spinal cord-mediated neuroinflammation after spinal cord injury. ( A ) ELISA showed that, compared to the sham group, the expression of IL-1β and IL-18 in the spinal cord were significantly increased after spinal cord injury (** P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

    2) Product Images from "Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway"

    Article Title: Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway

    Journal: Journal of Inflammation Research

    doi: 10.2147/JIR.S299163

    The concentration of extracellular IL-18 and IL-1β in the medium. PUN reduced the release of pro-inflammatory factors into the culture supernatant (n=5). ## Indicate P
    Figure Legend Snippet: The concentration of extracellular IL-18 and IL-1β in the medium. PUN reduced the release of pro-inflammatory factors into the culture supernatant (n=5). ## Indicate P

    Techniques Used: Concentration Assay

    The concentrations of IL-1β and IL-18 in the medium determined with ELISA kits. J774A.1 cells were pretreated with NAC (10 mM) or PUN (100 μM) + NAC (10 mM), followed by treated with LPS for 5.5 h, ATP for half an hour. ## Indicates P
    Figure Legend Snippet: The concentrations of IL-1β and IL-18 in the medium determined with ELISA kits. J774A.1 cells were pretreated with NAC (10 mM) or PUN (100 μM) + NAC (10 mM), followed by treated with LPS for 5.5 h, ATP for half an hour. ## Indicates P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    3) Product Images from "Rapamycin-induced autophagy attenuates hormone-imbalance-induced chronic non-bacterial prostatitis in rats via the inhibition of NLRP3 inflammasome-mediated inflammation"

    Article Title: Rapamycin-induced autophagy attenuates hormone-imbalance-induced chronic non-bacterial prostatitis in rats via the inhibition of NLRP3 inflammasome-mediated inflammation

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2018.9683

    Levels of serum IL-1β and IL-18 in rats from different groups. The serum concentrations of (A) IL-1β and (B) IL-18, as revealed by ELISA, in rats from the three groups. Data are expressed as the mean ± standard deviation. *P
    Figure Legend Snippet: Levels of serum IL-1β and IL-18 in rats from different groups. The serum concentrations of (A) IL-1β and (B) IL-18, as revealed by ELISA, in rats from the three groups. Data are expressed as the mean ± standard deviation. *P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Standard Deviation

    4) Product Images from "Sevoflurane Alleviates Myocardial Ischemia Reperfusion Injury by Inhibiting P2X7-NLRP3 Mediated Pyroptosis"

    Article Title: Sevoflurane Alleviates Myocardial Ischemia Reperfusion Injury by Inhibiting P2X7-NLRP3 Mediated Pyroptosis

    Journal: Frontiers in Molecular Biosciences

    doi: 10.3389/fmolb.2021.768594

    Changes in vital signs and inflammatory factors in these three groups of patients (A) different general anesthetics on the changes of heart rate, blood pressure, RPP and PRQ in peri-anesthesia in the three groups (B) Changes of IL-18 at different time points at pre- and post-anesthesia.
    Figure Legend Snippet: Changes in vital signs and inflammatory factors in these three groups of patients (A) different general anesthetics on the changes of heart rate, blood pressure, RPP and PRQ in peri-anesthesia in the three groups (B) Changes of IL-18 at different time points at pre- and post-anesthesia.

    Techniques Used:

    Sevoflurane alleviates inflammatory cell infiltration in MIRI rats (A) The expression of CD11b in rat myocardial tissue determined by immunofluorescence staining (n = 6,Scale bars 20 um) (B) Effects of Sevoflurane at different concentrations on the release of IL-1β and IL-18 in myocardial tissue after MIRI. All values are expressed as means ± SD (n = 6). * p
    Figure Legend Snippet: Sevoflurane alleviates inflammatory cell infiltration in MIRI rats (A) The expression of CD11b in rat myocardial tissue determined by immunofluorescence staining (n = 6,Scale bars 20 um) (B) Effects of Sevoflurane at different concentrations on the release of IL-1β and IL-18 in myocardial tissue after MIRI. All values are expressed as means ± SD (n = 6). * p

    Techniques Used: Expressing, Immunofluorescence, Staining

    5) Product Images from "Micheliolide Attenuates Lipopolysaccharide-Induced Inflammation by Modulating the mROS/NF-κB/NLRP3 Axis in Renal Tubular Epithelial Cells"

    Article Title: Micheliolide Attenuates Lipopolysaccharide-Induced Inflammation by Modulating the mROS/NF-κB/NLRP3 Axis in Renal Tubular Epithelial Cells

    Journal: Mediators of Inflammation

    doi: 10.1155/2020/3934769

    MCL inhibits LPS+ATP-induced activation of the NLRP3 inflammasome in NRK-52E cells. (a, b) Western blot analysis of the NLRP3 expression and its relative expression levels normalized to β -actin (ACTB). (c, d) Western blot analysis of the caspase-1 p10 expression and its relative expression levels normalized to α -tubulin. (e, f) Western blot analysis of the IL-1 β expression and its relative expression levels normalized to α -tubulin. (g) Real-time PCR analysis of IL-1 β expression in renal tubular epithelial cells. (h, i) Western blot analysis of the IL-18 expression and its relative expression levels normalized to ACTB. (j) ELISA analysis of IL-18 expression in each group. Data are presented as the mean ± SEM. ∗ P
    Figure Legend Snippet: MCL inhibits LPS+ATP-induced activation of the NLRP3 inflammasome in NRK-52E cells. (a, b) Western blot analysis of the NLRP3 expression and its relative expression levels normalized to β -actin (ACTB). (c, d) Western blot analysis of the caspase-1 p10 expression and its relative expression levels normalized to α -tubulin. (e, f) Western blot analysis of the IL-1 β expression and its relative expression levels normalized to α -tubulin. (g) Real-time PCR analysis of IL-1 β expression in renal tubular epithelial cells. (h, i) Western blot analysis of the IL-18 expression and its relative expression levels normalized to ACTB. (j) ELISA analysis of IL-18 expression in each group. Data are presented as the mean ± SEM. ∗ P

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

    6) Product Images from "Suppression of lncRNA NLRP3 inhibits NLRP3-triggered inflammatory responses in early acute lung injury"

    Article Title: Suppression of lncRNA NLRP3 inhibits NLRP3-triggered inflammatory responses in early acute lung injury

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-021-04180-y

    miR-138-5p regulates the inflammatory response by targeting NLRP3. A The predicted miR-138-5p-binding sites in the NLRP3 mRNA 3′-UTR. B A firefly luciferase reporter containing either wild-type or mutant NLRP3 was cotransfected into NR8383 AM cells with miR-138-5p mimics NC or miR-138-5p mimics. qRT-PCR assays were used to analyse the mRNA expression of C miR-138-5p, D NLRP3, E Caspase-1, F IL-18, and G IL-1β in the NR8383 AM cells ( n = 6). β-Actin was used as a reference gene. H , I ELISA was used to analyse the IL-1β and IL-18 levels in the culture supernatants. J Western blotting assay of the protein expression levels of NLRP3 and Caspase-1. K , L Cell apoptosis was determined by Hoechst 33342 and PI dual staining assays ( K ) and counted ( L ). The data are presented as mean ± SE ( n = 6). * P
    Figure Legend Snippet: miR-138-5p regulates the inflammatory response by targeting NLRP3. A The predicted miR-138-5p-binding sites in the NLRP3 mRNA 3′-UTR. B A firefly luciferase reporter containing either wild-type or mutant NLRP3 was cotransfected into NR8383 AM cells with miR-138-5p mimics NC or miR-138-5p mimics. qRT-PCR assays were used to analyse the mRNA expression of C miR-138-5p, D NLRP3, E Caspase-1, F IL-18, and G IL-1β in the NR8383 AM cells ( n = 6). β-Actin was used as a reference gene. H , I ELISA was used to analyse the IL-1β and IL-18 levels in the culture supernatants. J Western blotting assay of the protein expression levels of NLRP3 and Caspase-1. K , L Cell apoptosis was determined by Hoechst 33342 and PI dual staining assays ( K ) and counted ( L ). The data are presented as mean ± SE ( n = 6). * P

    Techniques Used: Binding Assay, Luciferase, Mutagenesis, Quantitative RT-PCR, Expressing, Enzyme-linked Immunosorbent Assay, Western Blot, Staining

    The mechanism by which the lncRNA NLRP3/miR-138-5p/NLRP3 ceRNET functions in the inflammatory response. The lungs of rats were injected with PBS in the control group and LPS-treated rats were further treated with si-r-lncRNA NLRP3, Lv-lncRNA NLRP3, agomiR-138-5p, antagomiR-138-5p, Lv-lncRNA NLRP3 + agomiR-138-5p, and si-r-lnc NLRP3 + antagomiR-138-5p. A Morphometric changes in the appearance of the lungs that had been fixed in 4% paraformaldehyde for 24 h at 25 °C in each group. B , C The protein expression levels of NLRP3 and caspase-1 in rat lung tissues. qRT-PCR assays were used to analyse mRNA expression of D lncRNA NLRP3, E NLRP3, F IL-18, G Caspase-1, H IL-1β, and I miR-138-5p in the lung tissues of rats. ELISA analysis of the IL-1β ( J ) and IL-18 ( K ) levels in the culture supernatant. L Graphical summary of the role of the lncRNA NLRP3/miR-138-5p/NLRP3 ceRNET in acute lung injury. β-Actin was used as the reference. The data are presented as mean ± SE ( n = 6). * P
    Figure Legend Snippet: The mechanism by which the lncRNA NLRP3/miR-138-5p/NLRP3 ceRNET functions in the inflammatory response. The lungs of rats were injected with PBS in the control group and LPS-treated rats were further treated with si-r-lncRNA NLRP3, Lv-lncRNA NLRP3, agomiR-138-5p, antagomiR-138-5p, Lv-lncRNA NLRP3 + agomiR-138-5p, and si-r-lnc NLRP3 + antagomiR-138-5p. A Morphometric changes in the appearance of the lungs that had been fixed in 4% paraformaldehyde for 24 h at 25 °C in each group. B , C The protein expression levels of NLRP3 and caspase-1 in rat lung tissues. qRT-PCR assays were used to analyse mRNA expression of D lncRNA NLRP3, E NLRP3, F IL-18, G Caspase-1, H IL-1β, and I miR-138-5p in the lung tissues of rats. ELISA analysis of the IL-1β ( J ) and IL-18 ( K ) levels in the culture supernatant. L Graphical summary of the role of the lncRNA NLRP3/miR-138-5p/NLRP3 ceRNET in acute lung injury. β-Actin was used as the reference. The data are presented as mean ± SE ( n = 6). * P

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

    LncRNA NLRP3 regulates the inflammatory response through the lncRNA NLRP3/miR-138-5p/NLRP3 ceRNET in vitro. miR-138-5p suppression reversed the effects of silncRNA NLRP3 on the mRNA expression of A lncRNA NLRP3, B NLRP3, C Caspase-1, D IL-1β, E IL-18, and F miR-138-5p in NR8383 alveolar macrophage (AMs) cells. β-Actin was used as the reference gene. G , H ELISA analysis of the IL-1β and IL-18 levels in the culture supernatant. I Western blotting assay of the protein expression levels of NLRP3 and caspase-1. J , K Cell apoptosis was determined by Hoechst 33342 and PI dual staining assays ( J ) and counted ( K ). The data are presented as mean ± SE ( n = 6). * P
    Figure Legend Snippet: LncRNA NLRP3 regulates the inflammatory response through the lncRNA NLRP3/miR-138-5p/NLRP3 ceRNET in vitro. miR-138-5p suppression reversed the effects of silncRNA NLRP3 on the mRNA expression of A lncRNA NLRP3, B NLRP3, C Caspase-1, D IL-1β, E IL-18, and F miR-138-5p in NR8383 alveolar macrophage (AMs) cells. β-Actin was used as the reference gene. G , H ELISA analysis of the IL-1β and IL-18 levels in the culture supernatant. I Western blotting assay of the protein expression levels of NLRP3 and caspase-1. J , K Cell apoptosis was determined by Hoechst 33342 and PI dual staining assays ( J ) and counted ( K ). The data are presented as mean ± SE ( n = 6). * P

    Techniques Used: In Vitro, Expressing, Affinity Magnetic Separation, Enzyme-linked Immunosorbent Assay, Western Blot, Staining

    Effects of LPS on the lncRNA NLRP3, miR-138-5p, NLRP3, Caspase-1, IL-1β, and IL-18 expression levels in early ALI. A qRT-PCR assay was used to analyse the mRNA expression of A LncRNA NLRP3, B miR-138-5p, C NLRP3, D Caspase-1, E IL-1β, and F IL-18 in LPS-induced ALI. β-Actin was used as the reference gene. G , H ELISA analysis of the IL-1β and IL-18 levels in the culture supernatant. Cell apoptosis was determined by Hoechst 33342 and PI dual staining assays ( I ) and counted ( J ). The expression of NLRP3 and caspase-1 in the NR8383 AM cells from the four groups was analysed by western blotting ( K ). L Expression trends of lncRNA NLRP3, NLRP3, caspase-1, IL-1β, IL-18, and miR-138-5p in the negative control group and groups treated with LPS for 6, 12, and 24 h. The data are presented as mean ± SE ( n = 6). * P
    Figure Legend Snippet: Effects of LPS on the lncRNA NLRP3, miR-138-5p, NLRP3, Caspase-1, IL-1β, and IL-18 expression levels in early ALI. A qRT-PCR assay was used to analyse the mRNA expression of A LncRNA NLRP3, B miR-138-5p, C NLRP3, D Caspase-1, E IL-1β, and F IL-18 in LPS-induced ALI. β-Actin was used as the reference gene. G , H ELISA analysis of the IL-1β and IL-18 levels in the culture supernatant. Cell apoptosis was determined by Hoechst 33342 and PI dual staining assays ( I ) and counted ( J ). The expression of NLRP3 and caspase-1 in the NR8383 AM cells from the four groups was analysed by western blotting ( K ). L Expression trends of lncRNA NLRP3, NLRP3, caspase-1, IL-1β, IL-18, and miR-138-5p in the negative control group and groups treated with LPS for 6, 12, and 24 h. The data are presented as mean ± SE ( n = 6). * P

    Techniques Used: Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Staining, Western Blot, Negative Control

    LncRNA NLRP3 regulates the inflammatory response during ALI through NLRP3 inflammasomes. A qRT-PCR assay was used to analyse the mRNA expression of A lncRNA NLRP3, B NLRP3, C Caspase-1, D IL-18, E IL-1β, and F miR-138-5p in LPS -induced ALI. β-Actin was used as the reference gene. G , H ELISA was used to analyse the IL-1β and IL-18 levels in the culture supernatants. I , J Cell apoptosis was determined by Hoechst 33342 and PI dual staining assays ( I ) and counted ( J ). K Western blotting was used to analyse the protein expression of NLRP3 and caspase-1 after lncRNA NLRP3 overexpression in the cytoplasm. The data are presented as mean ± SE ( n = 6). * P
    Figure Legend Snippet: LncRNA NLRP3 regulates the inflammatory response during ALI through NLRP3 inflammasomes. A qRT-PCR assay was used to analyse the mRNA expression of A lncRNA NLRP3, B NLRP3, C Caspase-1, D IL-18, E IL-1β, and F miR-138-5p in LPS -induced ALI. β-Actin was used as the reference gene. G , H ELISA was used to analyse the IL-1β and IL-18 levels in the culture supernatants. I , J Cell apoptosis was determined by Hoechst 33342 and PI dual staining assays ( I ) and counted ( J ). K Western blotting was used to analyse the protein expression of NLRP3 and caspase-1 after lncRNA NLRP3 overexpression in the cytoplasm. The data are presented as mean ± SE ( n = 6). * P

    Techniques Used: Quantitative RT-PCR, Expressing, Enzyme-linked Immunosorbent Assay, Staining, Western Blot, Over Expression

    7) Product Images from "Dexmedetomidine attenuates myocardial ischemia-reperfusion injury in vitro by inhibiting NLRP3 Inflammasome activation"

    Article Title: Dexmedetomidine attenuates myocardial ischemia-reperfusion injury in vitro by inhibiting NLRP3 Inflammasome activation

    Journal: BMC Anesthesiology

    doi: 10.1186/s12871-021-01334-5

    Effects of DEX on inflammation and the NLRP3 inflammasome in H/R injury. a The levels of TNF-α were determined in CF supernatant by ELISA. b The levels of IL-18 were determined in CF supernatant by ELISA. c The mRNA levels of IL-1β, IL-18, TNF-α, NLRP3, Caspase1, and ASC in CFs treated with DEX, MCC950 and DEX + MCC950 examined by RT-qPCR. d The densitometric value of NLRP3, Caspase1, cleaved caspase-1, ASC and IL-1β protein bands in CFs treated with DEX, MCC950 and DEX + MCC950 examined by western blot assay. Full-length blots are presented in Supplementary Fig. 1–6). e The protein levels of NLRP3, Caspase1, cleaved caspase-1, ASC and IL-1β in CFs treated with DEX, MCC950 and DEX + MCC950 examined by western blot analysis. * P
    Figure Legend Snippet: Effects of DEX on inflammation and the NLRP3 inflammasome in H/R injury. a The levels of TNF-α were determined in CF supernatant by ELISA. b The levels of IL-18 were determined in CF supernatant by ELISA. c The mRNA levels of IL-1β, IL-18, TNF-α, NLRP3, Caspase1, and ASC in CFs treated with DEX, MCC950 and DEX + MCC950 examined by RT-qPCR. d The densitometric value of NLRP3, Caspase1, cleaved caspase-1, ASC and IL-1β protein bands in CFs treated with DEX, MCC950 and DEX + MCC950 examined by western blot assay. Full-length blots are presented in Supplementary Fig. 1–6). e The protein levels of NLRP3, Caspase1, cleaved caspase-1, ASC and IL-1β in CFs treated with DEX, MCC950 and DEX + MCC950 examined by western blot analysis. * P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Western Blot

    8) Product Images from "Astaxanthin alleviates spinal cord ischemia-reperfusion injury via activation of PI3K/Akt/GSK-3β pathway in rats"

    Article Title: Astaxanthin alleviates spinal cord ischemia-reperfusion injury via activation of PI3K/Akt/GSK-3β pathway in rats

    Journal: Journal of Orthopaedic Surgery and Research

    doi: 10.1186/s13018-020-01790-8

    AST partially inhibited proinflammatory cytokines at 72 h after SCII. The levels of IL-1β ( a ), TNF-α ( b ), and IL-18 ( c ) were substantially increased, and IL-10 ( d ) was decreased in the SCII group compared with the sham group. Although pretreatment with AST could moderately reverse the above changes in cytokines, only the level of TNF-α was significantly decreased. Values are mean ± SD ( n = 6/group). * P
    Figure Legend Snippet: AST partially inhibited proinflammatory cytokines at 72 h after SCII. The levels of IL-1β ( a ), TNF-α ( b ), and IL-18 ( c ) were substantially increased, and IL-10 ( d ) was decreased in the SCII group compared with the sham group. Although pretreatment with AST could moderately reverse the above changes in cytokines, only the level of TNF-α was significantly decreased. Values are mean ± SD ( n = 6/group). * P

    Techniques Used: AST Assay

    9) Product Images from "Dicer1 is reduced in APPswe/PSEN1dE9 mice and is regulated by Nrf2"

    Article Title: Dicer1 is reduced in APPswe/PSEN1dE9 mice and is regulated by Nrf2

    Journal: bioRxiv

    doi: 10.1101/711572

    knocking down Dicer 1 induced production of reactive oxygen species (ROS), reduced mitochondrial membrane potential, enhanced secretion of IL-1β, IL-18, and apoptosis in primary cultured neurons. (A) Primary murine cortical neurons (CNs) and hippocampal neurons (HNs) in 6-well plates were transfected with Dicer1 siRNA (50 pM) or control siRNA duplex (50 pM) per well by lipofectamine 2000 for 12 h in DMEM/F12 plus 2% B27. The medium was replaced with fresh neurobasal supplemented with 2% B27 and continued to be cultured for 36 h. The effects of knockdown by Dicer1 siRNA were normalized to those of NC siRNA and averaged from three independent culture preparation. Student’s t - test was used to compare the differences, **p=0.0025 for comparison in CNs and *p=0.044 for comparison in HNs for Dicer 1. ( B ) The ROS levels in CNs or HNs were measured by incubating 2’,7’-dichlorodihydrofluorescein diacetate for 20 min at 37 °C. The fluorescence values in relative fluorescence units (RFU) were acquired in a plate reader at 485 nm and were averaged from four independent culture preparation with duplicate cultures in each preparation. Student’s t-test was used to compare the differences of ROS production in neurons between transfection with Dicer1 siRNA and control siRNA. ****p=0.00001 in CNs, ****p=0.00001 in HNs. (C) Representative images of JC-1 staining in CNs and HNs subject to Dicer1 knockdown as above, Bar 10 µm for all panels. (D) Mitochondrial membrane potential (Δm) of CNs and HNs subject to Dicer1 knockdown. The neurons were subject to Dicer1 knockdown thereof and mitochondria (30 µg) were isolated and stained with JC-1. The values of mitochondrial membrane potential (Δm) were indicated by the ratios between aggregated/monomer RFU and averaged from three independent culture preparations. Student’s t-test was used to compare the differences, *p=0.0369 in CNs, *p=0.0399 in HNs. (E, F) secreted IL-1β and IL-18 in CNs and HNs subject to Dicer1 knockdown. The CNs or HNs were subjected to Dicer1 knockdown as above. The culture media (100 µL) from neuronal culture subjected to transfection with Dicer1 siRNA or control siRNA duplex were collected and measured by ELISA. The concentrations of IL-1β and IL-18 were averaged from three independent culture preparation. Student’s t-test was used to compare the differences. *p=0.0381 when comparing IL-1β production in CNs and *p=0.0391 in HNs. *p=0.0331 when comparing IL-18 production in CNs and **p=0.007 in HNs. (G) Viability of neurons subjected to Dicer1 knockdown. CNs or HNs at the density of 5×10 3 were transfected with Dicer 1 siRNA and NC siRNA for 12 h in DMEM/F12 plus 2% B27, which was replaced with fresh neurobasal medium supplemented with 2% B27 and continued to be cultured for 36 h, respectively. The absorption values at OD 450nm in Dicer1 siRNA group were measured and normalized to NC siRNA group. Student’s t-test , **p=0.0028 for comparison in CNs, **p=0.0012 for comparison in HNs. (H) Representative images of Dicer 1, caspase3 and activated caspase3 in CNs and HNs subject to Dicer1 knockdown. βIII-tubulin was used as a loading control. (I) The optical densities of activated caspase-3 relative to βIII-tubulin from H were normalized to NC siRNA group, and averaged from three independent culture preparation. Student’s t-test was used to compare the differences, ***p=0.0008 for comparison in CNs and ***p=0.002 for comparison in HNs.
    Figure Legend Snippet: knocking down Dicer 1 induced production of reactive oxygen species (ROS), reduced mitochondrial membrane potential, enhanced secretion of IL-1β, IL-18, and apoptosis in primary cultured neurons. (A) Primary murine cortical neurons (CNs) and hippocampal neurons (HNs) in 6-well plates were transfected with Dicer1 siRNA (50 pM) or control siRNA duplex (50 pM) per well by lipofectamine 2000 for 12 h in DMEM/F12 plus 2% B27. The medium was replaced with fresh neurobasal supplemented with 2% B27 and continued to be cultured for 36 h. The effects of knockdown by Dicer1 siRNA were normalized to those of NC siRNA and averaged from three independent culture preparation. Student’s t - test was used to compare the differences, **p=0.0025 for comparison in CNs and *p=0.044 for comparison in HNs for Dicer 1. ( B ) The ROS levels in CNs or HNs were measured by incubating 2’,7’-dichlorodihydrofluorescein diacetate for 20 min at 37 °C. The fluorescence values in relative fluorescence units (RFU) were acquired in a plate reader at 485 nm and were averaged from four independent culture preparation with duplicate cultures in each preparation. Student’s t-test was used to compare the differences of ROS production in neurons between transfection with Dicer1 siRNA and control siRNA. ****p=0.00001 in CNs, ****p=0.00001 in HNs. (C) Representative images of JC-1 staining in CNs and HNs subject to Dicer1 knockdown as above, Bar 10 µm for all panels. (D) Mitochondrial membrane potential (Δm) of CNs and HNs subject to Dicer1 knockdown. The neurons were subject to Dicer1 knockdown thereof and mitochondria (30 µg) were isolated and stained with JC-1. The values of mitochondrial membrane potential (Δm) were indicated by the ratios between aggregated/monomer RFU and averaged from three independent culture preparations. Student’s t-test was used to compare the differences, *p=0.0369 in CNs, *p=0.0399 in HNs. (E, F) secreted IL-1β and IL-18 in CNs and HNs subject to Dicer1 knockdown. The CNs or HNs were subjected to Dicer1 knockdown as above. The culture media (100 µL) from neuronal culture subjected to transfection with Dicer1 siRNA or control siRNA duplex were collected and measured by ELISA. The concentrations of IL-1β and IL-18 were averaged from three independent culture preparation. Student’s t-test was used to compare the differences. *p=0.0381 when comparing IL-1β production in CNs and *p=0.0391 in HNs. *p=0.0331 when comparing IL-18 production in CNs and **p=0.007 in HNs. (G) Viability of neurons subjected to Dicer1 knockdown. CNs or HNs at the density of 5×10 3 were transfected with Dicer 1 siRNA and NC siRNA for 12 h in DMEM/F12 plus 2% B27, which was replaced with fresh neurobasal medium supplemented with 2% B27 and continued to be cultured for 36 h, respectively. The absorption values at OD 450nm in Dicer1 siRNA group were measured and normalized to NC siRNA group. Student’s t-test , **p=0.0028 for comparison in CNs, **p=0.0012 for comparison in HNs. (H) Representative images of Dicer 1, caspase3 and activated caspase3 in CNs and HNs subject to Dicer1 knockdown. βIII-tubulin was used as a loading control. (I) The optical densities of activated caspase-3 relative to βIII-tubulin from H were normalized to NC siRNA group, and averaged from three independent culture preparation. Student’s t-test was used to compare the differences, ***p=0.0008 for comparison in CNs and ***p=0.002 for comparison in HNs.

    Techniques Used: Cell Culture, Transfection, Fluorescence, Staining, Isolation, Enzyme-linked Immunosorbent Assay

    Overexpression of Dicer 1 reduced Aβ42 oligomer-mediated secretion of IL-1β and IL-18, apoptosis, and neurite deficit in primary hippocampal neuronal cultures. (A) The primary murine hippocampal neurons at DIV 3 were treated with Aβ42 oligomer (100 nM) for 24 h or subject to sham treatment in neurobasal medium plus 2% B27. In a parallel experiment, the medium was replaced with fresh neurobasal medium plus 2% B27 following Aβ42 treatment, and then infected with vehicle virus, Ad-EGFP or Ad-dicer1-T2A:EGFP virus (5 X 10 7 vg/mL) for 48 h. At the end of treatment, the cultures were harvested and homogenized for western blot against Dicer1, caspase 3, and activated caspase 3. βIII-tubulin was used as a loading control. (B) Dicer1 relative to βIII-tubulin were normalized to sham treatment and averaged from three independent culture preparation. One-way ANOVA followed by Tukey’s post hoc test was used to compare the differences. Dicer1 was reduced by Aβ42 oligomer treatment compared to sham treatment (*p=0.033) and the reduction of Dicer1 by Aβ42 was rescued by infection of Ad-dicer1-T2A:EGFP compared to infection by vehicle virus (**p=0.0074). (C) Activated caspase3 relative to βIII-tubulin were normalized to sham treatment and averaged from three independent culture preparation. One-way ANOVA followed by Tukey’s post hoc test was used to compare the differences. Activated caspase3 was increased by Aβ42 oligomer compared to sham treatment (**p=0.0061), which was reduced by infection of Ad-dicer1-T2A:EGFP compared to infection by vehicle virus (*p=0.023). (D) The loss of cell viability of hippocampal neurons treated by Aβ (***p=0.00067) was significantly rescued by infection with Ad-dicer1-T2A:EGFP compared to infection by vehicle virus (*p=0.047). The values were averaged from quadruplicate cultures with three independent culture preparation. The cultured media were also collected from the cultures treated as in A and subject to ELISA detection of IL-1β and IL-18. (E) Aβ42 oligomer treatment increased IL-1β in the supernatants (*p=0.023) which was reduced by infection of Ad-dicer1-T2A:EGFP compared to infection by vehicle virus (**p=0.005). The values were averaged from quadruplicate cultures with three independent cell preparation and One-way ANOVA followed by Tukey’s post hoc test was used to compare the differences. (F) The culture media were collected and subject to ELISA detection of IL-18 as in E. Aβ treatment increased IL-8 (*p=0.019) which was reduced by infection of Ad-dicer1-T2A:EGFP compared to infection by empty virus (*p=0.04). The values were averaged from quadruplicate cultures with three independent cell preparation and One-way ANOVA followed by Tukey’s post hoc test was used to compare the difference. (G) Representative hippocampal neurons (150 neurons for each type of treatment) infected by Ad-EGFP virus (Ad-EGFP), Aβ42 treatment followed by infection with Ad-EGFP virus (Aβ Ad-EGFP) and Aβ42 treatment followed by infection with Ad-Dicer1-T2A:EGFP virus (Aβ Ad-Dicer1:T2A:EGFP) were indicated. (H) Neurite lengths of hippocampal neurons with treatment from G were calculated and averaged. Aβ42 treatment reduced neurite length compared to sham treatment (*p=0.025) which was rescued by infection with Ad-dicer 1-T2A:EGFP virus (*p=0.047). The neurite length averaged from 150 neurons in each treatment and One-way ANOVA followed by Tukey’s post hoc test was used to compare the differences.
    Figure Legend Snippet: Overexpression of Dicer 1 reduced Aβ42 oligomer-mediated secretion of IL-1β and IL-18, apoptosis, and neurite deficit in primary hippocampal neuronal cultures. (A) The primary murine hippocampal neurons at DIV 3 were treated with Aβ42 oligomer (100 nM) for 24 h or subject to sham treatment in neurobasal medium plus 2% B27. In a parallel experiment, the medium was replaced with fresh neurobasal medium plus 2% B27 following Aβ42 treatment, and then infected with vehicle virus, Ad-EGFP or Ad-dicer1-T2A:EGFP virus (5 X 10 7 vg/mL) for 48 h. At the end of treatment, the cultures were harvested and homogenized for western blot against Dicer1, caspase 3, and activated caspase 3. βIII-tubulin was used as a loading control. (B) Dicer1 relative to βIII-tubulin were normalized to sham treatment and averaged from three independent culture preparation. One-way ANOVA followed by Tukey’s post hoc test was used to compare the differences. Dicer1 was reduced by Aβ42 oligomer treatment compared to sham treatment (*p=0.033) and the reduction of Dicer1 by Aβ42 was rescued by infection of Ad-dicer1-T2A:EGFP compared to infection by vehicle virus (**p=0.0074). (C) Activated caspase3 relative to βIII-tubulin were normalized to sham treatment and averaged from three independent culture preparation. One-way ANOVA followed by Tukey’s post hoc test was used to compare the differences. Activated caspase3 was increased by Aβ42 oligomer compared to sham treatment (**p=0.0061), which was reduced by infection of Ad-dicer1-T2A:EGFP compared to infection by vehicle virus (*p=0.023). (D) The loss of cell viability of hippocampal neurons treated by Aβ (***p=0.00067) was significantly rescued by infection with Ad-dicer1-T2A:EGFP compared to infection by vehicle virus (*p=0.047). The values were averaged from quadruplicate cultures with three independent culture preparation. The cultured media were also collected from the cultures treated as in A and subject to ELISA detection of IL-1β and IL-18. (E) Aβ42 oligomer treatment increased IL-1β in the supernatants (*p=0.023) which was reduced by infection of Ad-dicer1-T2A:EGFP compared to infection by vehicle virus (**p=0.005). The values were averaged from quadruplicate cultures with three independent cell preparation and One-way ANOVA followed by Tukey’s post hoc test was used to compare the differences. (F) The culture media were collected and subject to ELISA detection of IL-18 as in E. Aβ treatment increased IL-8 (*p=0.019) which was reduced by infection of Ad-dicer1-T2A:EGFP compared to infection by empty virus (*p=0.04). The values were averaged from quadruplicate cultures with three independent cell preparation and One-way ANOVA followed by Tukey’s post hoc test was used to compare the difference. (G) Representative hippocampal neurons (150 neurons for each type of treatment) infected by Ad-EGFP virus (Ad-EGFP), Aβ42 treatment followed by infection with Ad-EGFP virus (Aβ Ad-EGFP) and Aβ42 treatment followed by infection with Ad-Dicer1-T2A:EGFP virus (Aβ Ad-Dicer1:T2A:EGFP) were indicated. (H) Neurite lengths of hippocampal neurons with treatment from G were calculated and averaged. Aβ42 treatment reduced neurite length compared to sham treatment (*p=0.025) which was rescued by infection with Ad-dicer 1-T2A:EGFP virus (*p=0.047). The neurite length averaged from 150 neurons in each treatment and One-way ANOVA followed by Tukey’s post hoc test was used to compare the differences.

    Techniques Used: Over Expression, Infection, Western Blot, Cell Culture, Enzyme-linked Immunosorbent Assay

    10) Product Images from "Rapamycin-induced autophagy attenuates hormone-imbalance-induced chronic non-bacterial prostatitis in rats via the inhibition of NLRP3 inflammasome-mediated inflammation"

    Article Title: Rapamycin-induced autophagy attenuates hormone-imbalance-induced chronic non-bacterial prostatitis in rats via the inhibition of NLRP3 inflammasome-mediated inflammation

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2018.9683

    Levels of serum IL-1β and IL-18 in rats from different groups. The serum concentrations of (A) IL-1β and (B) IL-18, as revealed by ELISA, in rats from the three groups. Data are expressed as the mean ± standard deviation. *P
    Figure Legend Snippet: Levels of serum IL-1β and IL-18 in rats from different groups. The serum concentrations of (A) IL-1β and (B) IL-18, as revealed by ELISA, in rats from the three groups. Data are expressed as the mean ± standard deviation. *P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Standard Deviation

    11) Product Images from "P2X7 Receptor (P2X7R) of Microglia Mediates Neuroinflammation by Regulating (NOD)-Like Receptor Protein 3 (NLRP3) Inflammasome-Dependent Inflammation After Spinal Cord Injury"

    Article Title: P2X7 Receptor (P2X7R) of Microglia Mediates Neuroinflammation by Regulating (NOD)-Like Receptor Protein 3 (NLRP3) Inflammasome-Dependent Inflammation After Spinal Cord Injury

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    doi: 10.12659/MSM.925491

    P2X7R of microglia in spinal cord-mediated neuroinflammation after spinal cord injury. ( A ) ELISA showed that, compared to the sham group, the expression of IL-1β and IL-18 in the spinal cord were significantly increased after spinal cord injury (** P
    Figure Legend Snippet: P2X7R of microglia in spinal cord-mediated neuroinflammation after spinal cord injury. ( A ) ELISA showed that, compared to the sham group, the expression of IL-1β and IL-18 in the spinal cord were significantly increased after spinal cord injury (** P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

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    Boster Bio rat il 1β elisa kit
    P2X7R of microglia in spinal cord-mediated neuroinflammation after spinal cord injury. ( A ) <t>ELISA</t> showed that, compared to the sham group, the expression of <t>IL-1β</t> and IL-18 in the spinal cord were significantly increased after spinal cord injury (** P
    Rat Il 1β Elisa Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    P2X7R of microglia in spinal cord-mediated neuroinflammation after spinal cord injury. ( A ) ELISA showed that, compared to the sham group, the expression of IL-1β and IL-18 in the spinal cord were significantly increased after spinal cord injury (** P

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: P2X7 Receptor (P2X7R) of Microglia Mediates Neuroinflammation by Regulating (NOD)-Like Receptor Protein 3 (NLRP3) Inflammasome-Dependent Inflammation After Spinal Cord Injury

    doi: 10.12659/MSM.925491

    Figure Lengend Snippet: P2X7R of microglia in spinal cord-mediated neuroinflammation after spinal cord injury. ( A ) ELISA showed that, compared to the sham group, the expression of IL-1β and IL-18 in the spinal cord were significantly increased after spinal cord injury (** P

    Article Snippet: The rat IL-1β ELISA kit (EK3711, BOSTER, Wuhan, China) and IL-18 ELISA kit (EK0592, BOSTER, Wuhan, China) were used to detect contents of IL-1β and IL-18 in the spinal cord segments according to the manufacturer’s instructions.

    Techniques: Enzyme-linked Immunosorbent Assay, Expressing

    The concentration of extracellular IL-18 and IL-1β in the medium. PUN reduced the release of pro-inflammatory factors into the culture supernatant (n=5). ## Indicate P

    Journal: Journal of Inflammation Research

    Article Title: Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway

    doi: 10.2147/JIR.S299163

    Figure Lengend Snippet: The concentration of extracellular IL-18 and IL-1β in the medium. PUN reduced the release of pro-inflammatory factors into the culture supernatant (n=5). ## Indicate P

    Article Snippet: Calcein-AM and PI were purchased from Tongren Chemical (Beijing, China); IL-1β and IL-18 kits were purchased from Boster Biological Technology (Wuhan, China).

    Techniques: Concentration Assay

    The concentrations of IL-1β and IL-18 in the medium determined with ELISA kits. J774A.1 cells were pretreated with NAC (10 mM) or PUN (100 μM) + NAC (10 mM), followed by treated with LPS for 5.5 h, ATP for half an hour. ## Indicates P

    Journal: Journal of Inflammation Research

    Article Title: Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway

    doi: 10.2147/JIR.S299163

    Figure Lengend Snippet: The concentrations of IL-1β and IL-18 in the medium determined with ELISA kits. J774A.1 cells were pretreated with NAC (10 mM) or PUN (100 μM) + NAC (10 mM), followed by treated with LPS for 5.5 h, ATP for half an hour. ## Indicates P

    Article Snippet: Calcein-AM and PI were purchased from Tongren Chemical (Beijing, China); IL-1β and IL-18 kits were purchased from Boster Biological Technology (Wuhan, China).

    Techniques: Enzyme-linked Immunosorbent Assay

    Levels of serum IL-1β and IL-18 in rats from different groups. The serum concentrations of (A) IL-1β and (B) IL-18, as revealed by ELISA, in rats from the three groups. Data are expressed as the mean ± standard deviation. *P

    Journal: Molecular Medicine Reports

    Article Title: Rapamycin-induced autophagy attenuates hormone-imbalance-induced chronic non-bacterial prostatitis in rats via the inhibition of NLRP3 inflammasome-mediated inflammation

    doi: 10.3892/mmr.2018.9683

    Figure Lengend Snippet: Levels of serum IL-1β and IL-18 in rats from different groups. The serum concentrations of (A) IL-1β and (B) IL-18, as revealed by ELISA, in rats from the three groups. Data are expressed as the mean ± standard deviation. *P

    Article Snippet: The serum levels of IL-1β (cat. no. EK0393) and IL-18 (cat. no. EK0592) were measured using a rat ELISA kit purchased from Wuhan Boster Biological Technology, Ltd. (Wuhan, China).

    Techniques: Enzyme-linked Immunosorbent Assay, Standard Deviation

    Changes in vital signs and inflammatory factors in these three groups of patients (A) different general anesthetics on the changes of heart rate, blood pressure, RPP and PRQ in peri-anesthesia in the three groups (B) Changes of IL-18 at different time points at pre- and post-anesthesia.

    Journal: Frontiers in Molecular Biosciences

    Article Title: Sevoflurane Alleviates Myocardial Ischemia Reperfusion Injury by Inhibiting P2X7-NLRP3 Mediated Pyroptosis

    doi: 10.3389/fmolb.2021.768594

    Figure Lengend Snippet: Changes in vital signs and inflammatory factors in these three groups of patients (A) different general anesthetics on the changes of heart rate, blood pressure, RPP and PRQ in peri-anesthesia in the three groups (B) Changes of IL-18 at different time points at pre- and post-anesthesia.

    Article Snippet: Ltd, Wuhan, China) and IL-18 ELISA Kit (Lot# 2002-6631,Wuhan Boster Biological Technology.

    Techniques:

    Sevoflurane alleviates inflammatory cell infiltration in MIRI rats (A) The expression of CD11b in rat myocardial tissue determined by immunofluorescence staining (n = 6,Scale bars 20 um) (B) Effects of Sevoflurane at different concentrations on the release of IL-1β and IL-18 in myocardial tissue after MIRI. All values are expressed as means ± SD (n = 6). * p

    Journal: Frontiers in Molecular Biosciences

    Article Title: Sevoflurane Alleviates Myocardial Ischemia Reperfusion Injury by Inhibiting P2X7-NLRP3 Mediated Pyroptosis

    doi: 10.3389/fmolb.2021.768594

    Figure Lengend Snippet: Sevoflurane alleviates inflammatory cell infiltration in MIRI rats (A) The expression of CD11b in rat myocardial tissue determined by immunofluorescence staining (n = 6,Scale bars 20 um) (B) Effects of Sevoflurane at different concentrations on the release of IL-1β and IL-18 in myocardial tissue after MIRI. All values are expressed as means ± SD (n = 6). * p

    Article Snippet: Ltd, Wuhan, China) and IL-18 ELISA Kit (Lot# 2002-6631,Wuhan Boster Biological Technology.

    Techniques: Expressing, Immunofluorescence, Staining