Anti-IL1 beta/IL1B Antibody Picoband®

Western blot analysis of IL1 beta using anti-IL1 beta antibody (PB9025).
Electrophoresis was performed on a 5-20% SDS-PAGE gel at 70V (Stacking gel) / 90V (Resolving gel) for 2-3 hours.
Lane 1: recombinant rat IL1 beta protein 10 ng,
Lane 2: recombinant rat IL1 beta protein 5 ng.
After electrophoresis, proteins were transferred to a nitrocellulose membrane at 150 mA for 50-90 minutes. Blocked the membrane with 5% non-fat milk/TBS for 1.5 hour at RT. The membrane was incubated with rabbit anti-IL1 beta antigen affinity purified polyclonal antibody (Catalog # PB9025) at 0.5 μg/mL overnight at 4°C, then washed with TBS-0.1%Tween 3 times with 5 minutes each and probed with a goat anti-rabbit IgG-HRP secondary antibody at a dilution of 1:5000 for 1.5 hour at RT. The signal is developed using an Enhanced Chemiluminescent detection (ECL) kit (Catalog # EK1002) with Tanon 5200 system. A specific band was detected for IL1 beta at approximately 17 kDa.

IHC analysis of IL1 beta using anti-IL1 beta antibody (PB9025).
IL1 beta was detected in a paraffin-embedded section of mouse spleen tissue. Heat mediated antigen retrieval was performed in EDTA buffer (pH 8.0, epitope retrieval solution). The tissue section was blocked with 10% goat serum. The tissue section was then incubated with 2 μg/ml rabbit anti-IL1 beta Antibody (PB9025) overnight at 4°C. Peroxidase Conjugated Goat Anti-rabbit IgG was used as secondary antibody and incubated for 30 minutes at 37°C. The tissue section was developed using HRP Conjugated Rabbit IgG Super Vision Assay Kit (Catalog # SV0002) with DAB as the chromogen.

Western blot analysis of IL1 beta using anti-IL1 beta antibody (PB9025).
Electrophoresis was performed on a 5-20% SDS-PAGE gel at 70V (Stacking gel) / 90V (Resolving gel) for 2-3 hours.The sample well of each lane was loaded with 30 ug of sample under reducing conditions.
Lane 1: mouse RAW264.7 whole cell lysates,
Lane 2: mouse RAW264.7 whole cell lysates.
After electrophoresis, proteins were transferred to a nitrocellulose membrane at 150 mA for 50-90 minutes. Blocked the membrane with 5% non-fat milk/TBS for 1.5 hour at RT. The membrane was incubated with rabbit anti-IL1 beta antigen affinity purified polyclonal antibody (Catalog # PB9025) at 0.5 μg/mL overnight at 4°C, then washed with TBS-0.1%Tween 3 times with 5 minutes each and probed with a goat anti-rabbit IgG-HRP secondary antibody at a dilution of 1:5000 for 1.5 hour at RT. The signal is developed using an Enhanced Chemiluminescent detection (ECL) kit (Catalog # EK1002) with Tanon 5200 system. A specific band was detected for IL1 beta at approximately 35 kDa.

IHC analysis of IL1 beta using anti-IL1 beta antibody (PB9025).
IL1 beta was detected in a paraffin-embedded section of rat spleen tissue. Heat mediated antigen retrieval was performed in EDTA buffer (pH 8.0, epitope retrieval solution). The tissue section was blocked with 10% goat serum. The tissue section was then incubated with 2 μg/ml rabbit anti-IL1 beta Antibody (PB9025) overnight at 4°C. Peroxidase Conjugated Goat Anti-rabbit IgG was used as secondary antibody and incubated for 30 minutes at 37°C. The tissue section was developed using HRP Conjugated Rabbit IgG Super Vision Assay Kit (Catalog # SV0002) with DAB as the chromogen.

TP corrected inflammation levels in the aging with DKD model rats. (A) Representative WB images and quantification of the expression of TNF‐α, IL‐1β, and IL‐18 ( n = 6). (B–D) Levels of TNF‐α, IL‐18, and IL‐1β in serum ( n = 6). (E) Representative WB images and quantification of the expression of IL‐4 and IL‐10 ( n = 6). (F, G) Levels of IL‐4 and IL‐10 in serum ( n = 6). Compared with the CON group, a p < 0.05; compared with the MOD group, b p < 0.05; compared with the TP‐L group, c p < 0.05; compared with the TP‐M group, d p < 0.05.
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SIRT1 agonist SRT1720 increased M2‐like macrophage and decreased lipid deposition by EGCG in the model cells. (A) Determination of the optimal concentration of SRT1720 ( n = 3). (B) Representative WB images and quantitative analysis of the level of iNOS, Arg‐1, SIRT1, IL‐4, P‐STAT6, and P‐AKT1 in the RAW264.7 cells ( n = 3). (C) Representative WB images and quantitative analysis of the level of SREBP‐1 and SREBP‐2 in the MPC5 cells ( n = 3). (D) Levels of TNF‐α, IL‐18, and IL‐1β in supernatant ( n = 6). (E, F) Levels of IL‐4 and IL‐10 in supernatant ( n = 6). Compared with the CON group, a p < 0.05; compared with the MOD group, b p < 0.05; compared with the EGCG group, c p < 0.05.
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DJ-1 regulated the disassociation of NLRX1 from TRAF6 after cerebral I/R injury via SHP-1. a , g After virus and TPI-1 were used to overexpress DJ-1 and inhibit SHP-1, respectively, Western blotting was used to detect NLRX1, TRAF6, and SHP-1 in rats. b , h After virus and TPI-1 were used to overexpress DJ-1 and inhibit SHP-1, respectively, Western blotting was used to detect NLRX1, TRAF6, and SHP-1 in astrocytes. c , i After treatment with an SHP-1 inhibitor, Western blotting was used to detect the cytokines IL-1β, IL-6, and TNF-α in rats. d , j After treatment with an SHP-1 inhibitor, Western blotting was used to detect the cytokines IL-1β, IL-6, and TNF-α in astrocytes. e Immunoprecipitation and immunoblot analyses of NLRX1-TRAF6 in rats. f Immunoprecipitation and immunoblot analyses of SHP-1-TRAF6 in rats. The data are expressed as the mean ± SEM. * p < 0.05 vs. the sham group; # p < 0.05 vs. the MCAO group; & p < 0.05 vs. the overexpression group; ★ p < 0.05 vs. the DMSO group; △ p < 0.05 vs. the DMSO group. n = 6 per group. The data are expressed as the mean ± SEM. * p < 0.05 vs. the control group; # p < 0.05 vs. the OGD/R group; & p < 0.05 vs. the overexpression group; ★ p < 0.05 vs. the DMSO group; △ p < 0.05 vs. the DMSO group. n = 6 per group
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SIRT1 inhibitor EX‐527 increased M1‐like macrophage and lipid accumulation by EGCG in the model cells. (A) Determination of the optimal concentration of EX‐527. n = 3. (B) Representative WB images and quantitative analysis of the level of iNOS, Arg‐1, SIRT1, IL‐4, P‐STAT6, and P‐AKT1 in the RAW264.7 cells. n = 3 (C) Representative WB images and quantitative analysis of the level of SREBP‐1 and SREBP‐2 in the MPC5 cells. n = 3. (D) Levels of TNF‐α, IL‐18, and IL‐1β in supernatant. n = 6. (E, F) Levels of IL‐4 and IL‐10 in supernatant. n = 6. Compared with the CON group, a p < 0.05; compared with the MOD group, b p < 0.05; compared with the EGCG group, c p < 0.05.
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DJ-1 interference increased the expression of TNF-α, IL-1β, and IL-6 after cerebral I/R injury. a and c Western blot detecting DJ-1 and the cytokines TNF-α, IL-1β, and IL-6 in rats. b , d Western blot detecting DJ-1 and the cytokines TNF-α, IL-1β, and IL-6 in astrocytes. e–g Quantification of TNF-α, IL-1β, and IL-6 in rats by ELISA. h‑j Quantification of TNF-α, IL-1β, and IL-6 in astrocytes by ELISA. The data are expressed as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. n = 6 per group
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DJ-1 inhibited the expression of TNF-α, IL-1β, and IL-6 after cerebral I/R injury via SHP-1. a , c After virus and TPI-1 were used to overexpress DJ-1 and inhibit SHP-1, respectively, Western blotting was used to detect the cytokines IL-1β, IL-6, and TNF-α in rats. b , d After virus and TPI-1 were used to overexpress DJ-1 and inhibit SHP-1, respectively, Western blotting was used to detect the cytokines IL-1β, IL-6, and TNF-α in astrocytes. e , g After treatment with an SHP-1 inhibitor, Western blotting was used to detect the cytokines IL-1β, IL-6, and TNF-α in rats. f , h After treatment with an SHP-1 inhibitor, Western blotting was used to detect the cytokines IL-1β, IL-6, and TNF-α in astrocytes. i , k , m Quantification of TNF-α, IL-1β, and IL-6 in rats by ELISA. j , l , n Quantification of TNF-α, IL-1β, and IL-6 in astrocytes by ELISA. The data are expressed as the mean ± SEM. * p < 0.05 vs. the sham group; # p < 0.05 vs. the MCAO group; & p < 0.05 vs. the overexpression group; ★ p < 0.05 vs. the DMSO group; △ p < 0.05 vs. the DMSO group; ◆ p < 0.05 vs. the TPI-1 group. n = 6 per group. The data are expressed as the mean ± SEM. * p < 0.05 vs. the control group; # p < 0.05 vs. the OGD/R group; & p < 0.05 vs. the overexpression group; ★ p < 0.05 vs. the DMSO group; △ p < 0.05 vs. the DMSO group; ◆ p < 0.05 vs. the TPI-1 group. n = 6 per group. The groups in a and b and their corresponding groups in the statistical graphs are as follows: sham (−−−), MCAO or OGD/R (+−−), scramble (+−−), overexpression (++−), overexpression + DMSO (++−), and overexpression + TPI-1 (+++). The groups in e and f and the corresponding groups in the statistical graphs are as follows: DMSO (+−−), TPI-1 (+−+), overexpression + DMSO (++−), overexpression + TPI-1 (+++)
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The pretreatment of RD-6 inhibited the IL-17 signaling pathway in indomethacin-induced GU rats. The expression of IL17RA, FOS, IL1B, and PTGS2 determined in gastric tissue by qRT-PCR (A) and western bloting (B) . Data are expressed as mean ± S.E.M ( n = 3). One-way ANOVA with the uncorrected Fisher’s LSD test was used to evaluate multiple comparisons. # p < 0.05, ## p < 0.01 vs. NC group; * p < 0.05, ** p < 0.01 vs. IND group. NC, normal control; IND, indomethacin; RD-6-L, M, and H represent Ruda-6 at low, medium and high doses, respectively.
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The pretreatment of RD-6 exerts anti-inflammatory effects against indomethacin-induced GU rats. The levels of IL-1β (A) , IL-6 (B) , IL-17 (C) , and PGE2 (D) in gastric tissue. Data are expressed as mean ± S.E.M ( n = 6). One-way ANOVA with the uncorrected Fisher’s LSD test was used to evaluate multiple comparisons. # p < 0.05, and ## p < 0.01 vs. the NC group; * p < 0.05, and ** p < 0.01 vs. the IND group. NC, normal control; IND, indomethacin; RAN, ranitidine; RD-6-L, M, and H represent Ruda-6 at low, medium and high doses, respectively.
Index in PubMed under a CC BY license. PMID: 37637418