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Increased IL-1β secretion by macrophages due to autophagy impairment enhances inflammatory chemokine expression in LSECs. ( A ) Protein expression in ATG7-KO macrophages and NC macrophages generated using the CRISPR-CAS9 system. ( B ) Evaluation of IL-1β and caspase-1 levels in the culture supernatant of THP-1 macrophages by ELISA following 24-hour stimulation with or without 25 ng/mL LPS (n = 3/group). ( C ) Experimental method using LPS-stimulated THP-1 macrophage conditioned medium. ( D ) Evaluation of NF-κB or MAP kinase-related proteins in TMNK-1 cells. ( E and F ) Inflammatory chemokine gene expression in TMNK-1 cells when treated with control medium or THP-1 macrophage conditioned medium (n = 4/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, <t>p38</t> <t>MAPK</t> inhibitor. ( G ) Inflammatory chemokine gene expression measured 24 hours after treating TMNK-1 cells with varying concentrations of human recombinant IL-1β (n = 4/group). ( H ) Evaluation of inflammatory chemokine expression in TMNK-1 cells after 6 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).
P38 Mapk Inhibitor Sb 203580, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress p38 mapk inhibitor adezmapimod
Increased IL-1β secretion by macrophages due to autophagy impairment enhances inflammatory chemokine expression in LSECs. ( A ) Protein expression in ATG7-KO macrophages and NC macrophages generated using the CRISPR-CAS9 system. ( B ) Evaluation of IL-1β and caspase-1 levels in the culture supernatant of THP-1 macrophages by ELISA following 24-hour stimulation with or without 25 ng/mL LPS (n = 3/group). ( C ) Experimental method using LPS-stimulated THP-1 macrophage conditioned medium. ( D ) Evaluation of NF-κB or MAP kinase-related proteins in TMNK-1 cells. ( E and F ) Inflammatory chemokine gene expression in TMNK-1 cells when treated with control medium or THP-1 macrophage conditioned medium (n = 4/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, <t>p38</t> <t>MAPK</t> inhibitor. ( G ) Inflammatory chemokine gene expression measured 24 hours after treating TMNK-1 cells with varying concentrations of human recombinant IL-1β (n = 4/group). ( H ) Evaluation of inflammatory chemokine expression in TMNK-1 cells after 6 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).
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Increased IL-1β secretion by macrophages due to autophagy impairment enhances inflammatory chemokine expression in LSECs. ( A ) Protein expression in ATG7-KO macrophages and NC macrophages generated using the CRISPR-CAS9 system. ( B ) Evaluation of IL-1β and caspase-1 levels in the culture supernatant of THP-1 macrophages by ELISA following 24-hour stimulation with or without 25 ng/mL LPS (n = 3/group). ( C ) Experimental method using LPS-stimulated THP-1 macrophage conditioned medium. ( D ) Evaluation of NF-κB or MAP kinase-related proteins in TMNK-1 cells. ( E and F ) Inflammatory chemokine gene expression in TMNK-1 cells when treated with control medium or THP-1 macrophage conditioned medium (n = 4/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, <t>p38</t> <t>MAPK</t> inhibitor. ( G ) Inflammatory chemokine gene expression measured 24 hours after treating TMNK-1 cells with varying concentrations of human recombinant IL-1β (n = 4/group). ( H ) Evaluation of inflammatory chemokine expression in TMNK-1 cells after 6 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).
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Increased IL-1β secretion by macrophages due to autophagy impairment enhances inflammatory chemokine expression in LSECs. ( A ) Protein expression in ATG7-KO macrophages and NC macrophages generated using the CRISPR-CAS9 system. ( B ) Evaluation of IL-1β and caspase-1 levels in the culture supernatant of THP-1 macrophages by ELISA following 24-hour stimulation with or without 25 ng/mL LPS (n = 3/group). ( C ) Experimental method using LPS-stimulated THP-1 macrophage conditioned medium. ( D ) Evaluation of NF-κB or MAP kinase-related proteins in TMNK-1 cells. ( E and F ) Inflammatory chemokine gene expression in TMNK-1 cells when treated with control medium or THP-1 macrophage conditioned medium (n = 4/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, p38 MAPK inhibitor. ( G ) Inflammatory chemokine gene expression measured 24 hours after treating TMNK-1 cells with varying concentrations of human recombinant IL-1β (n = 4/group). ( H ) Evaluation of inflammatory chemokine expression in TMNK-1 cells after 6 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Liver Sinusoidal Endothelial Cells Promote Metabolic Dysfunction-associated Steatohepatitis Progression via Interleukin-1R1-mediated Chemokine Production Induced by Macrophage-derived Interleukin-1β

doi: 10.1016/j.jcmgh.2025.101698

Figure Lengend Snippet: Increased IL-1β secretion by macrophages due to autophagy impairment enhances inflammatory chemokine expression in LSECs. ( A ) Protein expression in ATG7-KO macrophages and NC macrophages generated using the CRISPR-CAS9 system. ( B ) Evaluation of IL-1β and caspase-1 levels in the culture supernatant of THP-1 macrophages by ELISA following 24-hour stimulation with or without 25 ng/mL LPS (n = 3/group). ( C ) Experimental method using LPS-stimulated THP-1 macrophage conditioned medium. ( D ) Evaluation of NF-κB or MAP kinase-related proteins in TMNK-1 cells. ( E and F ) Inflammatory chemokine gene expression in TMNK-1 cells when treated with control medium or THP-1 macrophage conditioned medium (n = 4/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, p38 MAPK inhibitor. ( G ) Inflammatory chemokine gene expression measured 24 hours after treating TMNK-1 cells with varying concentrations of human recombinant IL-1β (n = 4/group). ( H ) Evaluation of inflammatory chemokine expression in TMNK-1 cells after 6 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).

Article Snippet: The inhibitors used were as follows: the NF-κB inhibitor SN50 (HY-P0151; MedChemExpress), the JNK inhibitor SP600125 (HY-12041; MedChemExpress), the p38 MAPK inhibitor SB 203580 (HY-10256; MedChemExpress), and the IL-1R antagonist (IL-1Ra) (093-05991; FUJIFILM Wako Pure Chemical Corporation).

Techniques: Expressing, Generated, CRISPR, Enzyme-linked Immunosorbent Assay, Gene Expression, Control, Recombinant

Macrophage-derived IL-1β increases CCL2 expression in HSCs via JNK activation. ( A ) Evaluation of the levels of NF-κB or MAPK-related proteins in LX-2 cells. ( B, C ) CCL2 gene expression in LX-2 cells treated with the control medium or THP-1 macrophage conditioned medium (n = 3/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, p38 MAPK inhibitor. ( D ) Evaluation of CCL2 expression in TMNK-1 cells after 48 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Liver Sinusoidal Endothelial Cells Promote Metabolic Dysfunction-associated Steatohepatitis Progression via Interleukin-1R1-mediated Chemokine Production Induced by Macrophage-derived Interleukin-1β

doi: 10.1016/j.jcmgh.2025.101698

Figure Lengend Snippet: Macrophage-derived IL-1β increases CCL2 expression in HSCs via JNK activation. ( A ) Evaluation of the levels of NF-κB or MAPK-related proteins in LX-2 cells. ( B, C ) CCL2 gene expression in LX-2 cells treated with the control medium or THP-1 macrophage conditioned medium (n = 3/group). SN50, NF-κB inhibitor; SP600125, JNK inhibitor; SB203580, p38 MAPK inhibitor. ( D ) Evaluation of CCL2 expression in TMNK-1 cells after 48 hours of stimulation with recombinant human IL-1β (5 ng/mL) in the presence of SP600125 and SB203580 (n = 4/group).

Article Snippet: The inhibitors used were as follows: the NF-κB inhibitor SN50 (HY-P0151; MedChemExpress), the JNK inhibitor SP600125 (HY-12041; MedChemExpress), the p38 MAPK inhibitor SB 203580 (HY-10256; MedChemExpress), and the IL-1R antagonist (IL-1Ra) (093-05991; FUJIFILM Wako Pure Chemical Corporation).

Techniques: Derivative Assay, Expressing, Activation Assay, Gene Expression, Control, Recombinant