stat3 inhibitor s3i 201  (Selleck Chemicals)

Journal: Journal of Translational Medicine

Article Title: Short-chain fatty acid-producing bacterial strains attenuate experimental ulcerative colitis by promoting M2 macrophage polarization via JAK/STAT3/FOXO3 axis inactivation

doi: 10.1186/s12967-024-05122-w

Figure Lengend Snippet: Treatment with a mixture of seven short-chain fatty acid-producing bacterial strains (7-mix) and the resulting culture supernatant mixture (mix-sup) inhibits JAK/STAT3/FOXO3 pathway activation in macrophages. A-B . qRT-PCR analysis of the effect of 7-mix and mix-sup on the regulation of the JAK/STAT3/FOXO3 axis in colitic mice treated or not with clodronate (CLD) liposomes. C . Effect of 7-mix and mix-sup on the immunohistochemical expression of STAT3 and FOXO3 in colitic mice treated with CLD. D . Flow cytometry analysis of the effect of S3I-201 and fedratinib on macrophage polarization. E . qRT-PCR analysis of the effect of 7-mix, mix-sup, S3I-201, and fedratinib on the mRNA expression of JAK2, STAT3, and FOXO3 in LPS-treated RAW264.7 cells. F . Western blot analysis of the effect of 7-mix, mix-sup, S3I-201, and fedratinib on the protein expression of JAK2, p-JAK2, STAT3, p-STAT3, and FOXO3 in LPS-treated RAW264.7 cells. N = 3. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: To evaluate the effect of the STAT3 inhibitor S3I-201 (Abcam, UK) and the JAK2 inhibitor fedratinib (SAR302503, Selleck, China) on JAK/STAT3/FOXO3 signaling, cells were incubated with 7-mix (2 − 2 , namely 2.5 × 10 7 CFU), mix-sup (2 − 4 ), S3I-201 (50 µM), fedratinib (10 µM), or S3I-201 + fedratinib for 4 h.

Techniques: Activation Assay, Quantitative RT-PCR, Liposomes, Immunohistochemical staining, Expressing, Flow Cytometry, Western Blot

Journal: Journal of Translational Medicine

Article Title: Short-chain fatty acid-producing bacterial strains attenuate experimental ulcerative colitis by promoting M2 macrophage polarization via JAK/STAT3/FOXO3 axis inactivation

doi: 10.1186/s12967-024-05122-w

Figure Lengend Snippet: Schematic representation of the regulation of dextran sulfate sodium-induced colitis by short-chain fatty acid (SCFA)-producing bacterial strains and SCFAs. Colitis damages the gut barrier, inducing the activation of M1 macrophages, which produce pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α. In turn, SCFA-producing bacterial strains and SCFAs stimulate the activation of M2 macrophages, which produce anti-inflammatory cytokines (i.e., IL-10) to inhibit JAK/STAT3/FOXO3 axis activation and improve gut barrier function

Article Snippet: To evaluate the effect of the STAT3 inhibitor S3I-201 (Abcam, UK) and the JAK2 inhibitor fedratinib (SAR302503, Selleck, China) on JAK/STAT3/FOXO3 signaling, cells were incubated with 7-mix (2 − 2 , namely 2.5 × 10 7 CFU), mix-sup (2 − 4 ), S3I-201 (50 µM), fedratinib (10 µM), or S3I-201 + fedratinib for 4 h.

Techniques: Activation Assay

Journal: International Journal of Molecular Sciences

Article Title: Regulation of Cathelicidin Antimicrobial Peptide (CAMP) Gene Expression by TNFα and cfDNA in Adipocytes

doi: 10.3390/ijms242115820

Figure Lengend Snippet: TNFα-induced CAMP gene expression is antagonized by inhibitor of PI3K signaling: TNFα induces CAMP expression in 3T3-L1 adipocytes ( A ). Inhibition of the PI3K pathway by 5 µM LY294002 antagonizes TNFα-induced CAMP expression, whereas inhibition of the NF-κB (5 µM BAY11-7085) ( B ), STAT3 (50 µM S3I-201), MAPK (5 µM SB239063), and MEK-1/-2 (5 µM U0126) pathways does not inhibit TNFα-induced CAMP expression ( C ). Basal CAMP expression is not significantly modified by inhibition of classical signal transduction pathways ( D ) (* p < 0.05, ** p < 0.01). N = 9–18 samples were investigated. Gene expression levels are given in relative gene expression as compared to control.

Article Snippet: Furthermore, co-stimulation experiments were performed with 10 ng/mL TNFα and inhibitors of different signal transduction pathways (NF-κB inhibitor BAY-11 (5 mM), STAT3 inhibitor S3I-201 (50 mM), selective MAPK inhibitor SB239063 (5 mM), MEK-1/-2 inhibitor U0126 (5 mM), and phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 (5 mM), all purchased from Merck).

Techniques: Expressing, Inhibition, Modification, Transduction