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p38 mapk inhibitor sb203580  (MedChemExpress)


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    MedChemExpress p38 mapk inhibitor sb203580
    P38 Mapk Inhibitor Sb203580, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p38+inhibitor+sb+203580/SB+203580+sulfone/pmc13176019-57-19-23
    Average 94 stars, based on 5 article reviews
    p38 mapk inhibitor sb203580 - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    other:

    Article Title: mTOR contributes to endothelium-dependent vasorelaxation by promoting eNOS expression and preventing eNOS uncoupling
    Article Snippet: ROS scavenger N-acetylcysteine (HY-B0215), mitochondrial antioxidant MitoQ (HY-100116A), Nox inhibitor Apocynin (HY-N0088), XO inhibitor Allopurinol (HY-B0219), p38 inhibitor SB 203580 (HY-10256) and JNK inhibitor SP 600125 (HY-12041) were purchased from MCE.

    HAT Assay:

    Article Title: Effects of short-chain fatty acids in inhibiting HDAC and activating p38 MAPK are critical for promoting B10 cell generation and function
    Article Snippet: For B10 cell analysis, splenocytes, PBMCs, and purified B cells were cultured with 1 μg/ml human or murine CD40 mAb (BioLegend), 40 nM CpG-ODN 1826 (Invitrogen), 4 μg/ml CpG-ODN 2395 (Invitrogen), or 10 μg/ml LPS (Sigma) for 2–4 days and stimulated with L + PIM for cytokine production at 5 h before cell harvest. .. In some experiments, cells were treated with inhibitors or metabolites, including HDACis TSA (1–10 nM; Beyotime) and vorinostat (100–500 nM; MCE), GPR41 agonist AR420626 (1–10 μM; APExBIO), GPR43 agonist (1–10 μM; Sigma-Aldrich) or antagonist GLPG0974 (500 nM; Sigma-Aldrich), GPR109A agonist niacin (1 mM; Sigma-Aldrich), HAT inhibitor anacardic acid (1–10 μM; MCE), ERK1/2 inhibitor U0126 (5 μM; MCE), p38 inhibitor SB 203580 (5 μM; MCE), or JNK inhibitor SP600125 (1 μM; MCE). .. A total of 1 × 10 7 /ml B cell-depleted splenocytes or purified B cells resuspended in PBS were labeled with 2 μM CFSE (BioLegend) for 15 min at 37 °C and then washed twice with complete RPMI-1640 medium for culture.



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    p38 mapk inhibitor sb203580  (MedChemExpress)
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    p38 mapk inhibitor sb 203580  (MedChemExpress)
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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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    p38 inhibitor  (Tocris)
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    Geum japonicum inhibits platelet aggregation by inhibiting PI3K/Akt and MAPK pathways. Platelets were induced aggregation with collagen, and the platelets were collected. Protein was extracted, and the expression of proteins related to platelet activation was investigated. Representative blots were presented in (A) . The expression of phospho-PI3K (B) , phospho-Akt (C) , phospho-ERK (D) , phospho-JNK (E) and <t>phospho-p38</t> (F) were normalized against their total forms. Expression of VASPser 239 (G) and VASPser 157 (H) were normalized against the total form of VASP. β-Actin was used as a housekeeping gene. The experiment was conducted in triplicate, and the blots were quantified using ImageJ. ERK inhibitor (PD98059), p38 inhibitor <t>(SB203580),</t> JNK inhibitor (SP600125), and PI3K inhibitor (LY294002) were used as a positive control. Data were presented as mean ± SD, and * P < 0.05, ** P < 0.01 and *** P < 0.001 was considered statistically significant against collagen-treated group. # P < 0.05, ## P < 0.01 and ### P < 0.001 were considered statistically significant against the resting group. Experiments were conducted in triplicate. R, Resting, C, collagen.
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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

    Geum japonicum inhibits platelet aggregation by inhibiting PI3K/Akt and MAPK pathways. Platelets were induced aggregation with collagen, and the platelets were collected. Protein was extracted, and the expression of proteins related to platelet activation was investigated. Representative blots were presented in (A) . The expression of phospho-PI3K (B) , phospho-Akt (C) , phospho-ERK (D) , phospho-JNK (E) and phospho-p38 (F) were normalized against their total forms. Expression of VASPser 239 (G) and VASPser 157 (H) were normalized against the total form of VASP. β-Actin was used as a housekeeping gene. The experiment was conducted in triplicate, and the blots were quantified using ImageJ. ERK inhibitor (PD98059), p38 inhibitor (SB203580), JNK inhibitor (SP600125), and PI3K inhibitor (LY294002) were used as a positive control. Data were presented as mean ± SD, and * P < 0.05, ** P < 0.01 and *** P < 0.001 was considered statistically significant against collagen-treated group. # P < 0.05, ## P < 0.01 and ### P < 0.001 were considered statistically significant against the resting group. Experiments were conducted in triplicate. R, Resting, C, collagen.

    Journal: Frontiers in Pharmacology

    Article Title: Geum japonicum Thunb. exhibits anti-platelet activity via the regulation of cyclic guanosine monophosphate

    doi: 10.3389/fphar.2025.1538417

    Figure Lengend Snippet: Geum japonicum inhibits platelet aggregation by inhibiting PI3K/Akt and MAPK pathways. Platelets were induced aggregation with collagen, and the platelets were collected. Protein was extracted, and the expression of proteins related to platelet activation was investigated. Representative blots were presented in (A) . The expression of phospho-PI3K (B) , phospho-Akt (C) , phospho-ERK (D) , phospho-JNK (E) and phospho-p38 (F) were normalized against their total forms. Expression of VASPser 239 (G) and VASPser 157 (H) were normalized against the total form of VASP. β-Actin was used as a housekeeping gene. The experiment was conducted in triplicate, and the blots were quantified using ImageJ. ERK inhibitor (PD98059), p38 inhibitor (SB203580), JNK inhibitor (SP600125), and PI3K inhibitor (LY294002) were used as a positive control. Data were presented as mean ± SD, and * P < 0.05, ** P < 0.01 and *** P < 0.001 was considered statistically significant against collagen-treated group. # P < 0.05, ## P < 0.01 and ### P < 0.001 were considered statistically significant against the resting group. Experiments were conducted in triplicate. R, Resting, C, collagen.

    Article Snippet: ERK inhibitor (PD98059), p38 inhibitor (SB203580), JNK inhibitor (SP600125), PI3K inhibitor (LY294002), and Rho kinase inhibitor (Y-27632) were acquired from Tocris Bioscience (Bristol, United Kingdom).

    Techniques: Expressing, Activation Assay, Positive Control