Journal: Microbiological research

Article Title: Melatonin attenuates chronic intermittent hypoxia-induced intestinal barrier dysfunction in mice.

doi: 10.1016/j.micres.2023.127480

Figure Lengend Snippet: Fig. 9. Melatonin attenuated Th17 differentiation during CIH in vitro. Naïve CD4+ T cells (CD3+ CD4+ CD45RA+ CD45RO-) from the spleens of healthy new-born mice were differentiated under Th17 conditions for 3 days under CIH in the presence of melatonin, a JAK2/STAT3 inhibitor, and a STAT3 activator. (A) Levels of IL- 17 A (a marker of Th17 cell expression) during in vitro differentiation. (B) Real time qRT-PCR analysis of the relative mRNA expression of STAT3 in naïve CD4+ T cells during in vitro polarization. (C) Representative flow cytometric plots of IL-17+ expression in gated CD4+ T cells under Th17 conditions. (D) Quantification of Th17 cells in the CON, CIH, CIH + MT, CIH + JAK2/STAT3 inhibitor, and CIH + MT + STAT3 activator groups (n = 4 per group). Data are expressed as mean ± SD. Group differences were assessed using ANOVA. * p < 0.05, * * p < 0.01, and * ** p < 0.001 for comparisons between the CON and CIH groups. #p < 0.05, ##p < 0.01, and ###p < 0.001 for comparisons between the CIH group and CIH + MT, CIH + JAK2/STAT3 inhibitor, and CIH + MT + STAT3 activator groups.

Article Snippet: CIH was induced in identical cell culture chambers (Oxycycler model C42; BioSpherix) for 48 h. As described previously (Philippe et al., 2015), hypoxia was induced with 0.5–1% O2 for 30 min followed by 21% O2 for 30 min. To further confirm the roles of melatonin and JAK2/STAT3 signalling in Caco-2 cells exposed to CIH, melatonin (20 ng/mL), the JAK2/STAT3 inhibitor FLLL32 (5 μM; 4434–05–3; Selleckchem, Houston, TX, USA) (Lin et al., 2010) and the STAT3 signal activator Colivelin (1 μM; 867021–83–8; Santa Cruz Biotechnology, Dallas, TX, USA) (Quévrain et al., 2016) were added to the culture medium before the CIH intervention.

Techniques: In Vitro, Marker, Expressing, Quantitative RT-PCR

Journal: Communications Biology

Article Title: p38α deficiency ameliorates psoriasis development by downregulating STAT3-mediated keratinocyte proliferation and cytokine production

doi: 10.1038/s42003-024-06700-w

Figure Lengend Snippet: a – c Primary KCs of WT and p38α ΔKC mice were stimulated with R848. R848 stimulation for 24 h to perform 5-ethynyl-2’-deoxyuridine (Edu) incorporation assay and calculate the frequency of Edu + cells ( a , n = 5-6). Scale bar: 100 μm. R848 stimulation for 5 h to determine the mRNA levels of inflammation-related genes and the relative expression was normalized with unstimulated KCs ( b , n = 4). R848 stimulation for indicated times to examine the activities of STAT3, p38, JNK, ERK, p65 and Akt ( c ). The numbers below the lanes indicate the band intensity relative to total protein. d Immunofluorescence staining of p-STAT3 in skin sections of WT and p38α ΔKC mice treated with IMQ for 3 days ( n = 4). Scale bar: 50 μm. e – j WT and p38α ΔKC mice topically treated with IMQ were intradermally injected with STAT3 activator Colivelin (Col) or control vehicle (Veh) ( n = 6): changes in ear thickness ( e ); disease severity score ( f ); histopathological changes in skin sections ( g ); infiltration of neutrophils ( h ); and relative expression of inflammation-related genes ( i ) in skin tissue; the frequencies of BrdU + KCs ( j ). Scale bar: 100 μm. All the assays were replicated three times with consistent results. Data represent mean ± SEM. Two-way ANOVA with Bonferroni post-tests ( a , f , h – j ), two-tailed Student’s t tests ( b ), and two-way ANOVA ( e ) were performed. * P < 0.05; ** P < 0.01; *** P < 0.001; ns not significant.

Article Snippet: In some experiments, IMQ-treated mice were intradermally injected with STAT3 activator Colivelin (Selleck) at a dose of 0.1 mg/kg body weight or STAT3 inhibitor S3I-201 (Selleck) at a dose of 0.5 mg/kg body weight on days 1, 3 and 5.

Techniques: Expressing, Immunofluorescence, Staining, Injection, Control, Two Tailed Test

Journal: Communications Biology

Article Title: p38α deficiency ameliorates psoriasis development by downregulating STAT3-mediated keratinocyte proliferation and cytokine production

doi: 10.1038/s42003-024-06700-w

Figure Lengend Snippet: a The activities of STAT3, p38, JNK, ERK, p65, and Akt were determined in WT and p38α ΔKC primary KCs stimulated with IL-17A for indicated times. The numbers below the lanes indicate the band intensity relative to total protein. b , c Primary KCs of WT and p38α ΔKC mice were pretreated with or without STAT3 activator Colivelin followed with or without stimulation of IL-17A. IL-17A stimulation for 24 h to perform the Edu incorporation assay and calculate the percentages of Edu + cells ( b , n = 5). Scale bar: 100 μm. IL-17A stimulation for 5 h to analyze the production of inflammation-related genes ( c , n = 4). d – g WT and p38α ΔKC mice were intradermally injected with IL-17A ( n = 6): changes in ear thickness ( d ); disease severity score ( e ); infiltration of neutrophils ( f ) and relative expression of inflammation-related genes ( g ) in skin tissue. All the assays were replicated three times with consistent results. Data represent mean ± SEM. Two-way ANOVA with Bonferroni post-tests ( b , c ), two-way ANOVA ( d ) and two-tailed Student’s t tests ( e – g ) were performed. * P < 0.05; ** P < 0.01; *** P < 0.001; ns not significant.

Article Snippet: In some experiments, IMQ-treated mice were intradermally injected with STAT3 activator Colivelin (Selleck) at a dose of 0.1 mg/kg body weight or STAT3 inhibitor S3I-201 (Selleck) at a dose of 0.5 mg/kg body weight on days 1, 3 and 5.

Techniques: Injection, Expressing, Two Tailed Test

Journal: Communications Biology

Article Title: p38α deficiency ameliorates psoriasis development by downregulating STAT3-mediated keratinocyte proliferation and cytokine production

doi: 10.1038/s42003-024-06700-w

Figure Lengend Snippet: a WT mice topically treated with IMQ for six consecutive days were intraperitoneally administered with the antibody against IL-17A (anti-IL-17A) or control IgG 4 h after IMQ treatment and the activities of p38 and STAT3 in KCs were analyzed by Western blot. b – f WT and p38α ΔKC mice topically treated with IMQ for six consecutive days were intradermally injected with STAT3 inhibitor S3I-201 or control vehicle at days 1, 3, and 5 ( n = 6): changes in ear thickness ( b ), disease severity score ( c ); histopathological changes in skin sections ( d ); infiltration of neutrophils ( e ) and relative expression of inflammation-related genes ( f ) in skin tissue. Scale bar: 100 μm. All the assays were replicated two times with consistent results. Data represent mean ± SEM. Two-way ANOVA ( b ) and two-way ANOVA with Bonferroni post-tests ( c , e , f ) were performed. ** P < 0.01; *** P < 0.001; ns not significant.

Article Snippet: In some experiments, IMQ-treated mice were intradermally injected with STAT3 activator Colivelin (Selleck) at a dose of 0.1 mg/kg body weight or STAT3 inhibitor S3I-201 (Selleck) at a dose of 0.5 mg/kg body weight on days 1, 3 and 5.

Techniques: Control, Western Blot, Injection, Expressing

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

Article Title: Esculetin Inhibits Proliferation, Invasion, and Migration of Laryngeal Cancer In Vitro and In Vivo by Inhibiting Janus Kinas (JAK)-Signal Transducer and Activator of Transcription-3 (STAT3) Activation

doi: 10.12659/MSM.916246

Figure Lengend Snippet: The effects of colivelin and C188-9 on esculetin-induced cell proliferation inhibition and p-STAT3 phosphorylation. Hep-2 cells were treated with 5 μM of esculetin and (or) colivelin (1 nM), and C188-9 (0.5 μM) for 48 h. ( A ) Cell viability of Hep-2 was assessed by MTT assay. ( B ) STAT3 phosphorylation in Hep-2 cells was modulated by single compound and combination of 2 compounds. Data represent the mean ±SD (* P<0.05, ** P<0.01).

Article Snippet: STAT3 inhibitor C188-9 was purchased from Selleck Chemicals (Houston, TX, USA) and the STAT3 activator colivelin was purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Inhibition, Phospho-proteomics, MTT Assay

Journal: Journal of Ovarian Research

Article Title: Obacunone alleviated the development of polycystic ovary syndrome via inhibiting STAT3 phosphorylation

doi: 10.1186/s13048-025-01934-6

Figure Lengend Snippet: Colivelin TFA reversed OB roles on apoptosis, inflammatory response and oxidative stress in DHEA-treated KGN cells. A Western blot for assessing p-STAT3 and STAT3 expression; ( B ) Flow cytometry was applied for detecting the apoptosis; ( C ) Western blot for assessing inflammatory factors expression; ( D ) DCFH-DA fluorescent probe for assessing ROS level; ( E ) The detection of MDA, GSH, SOD and CAT level. * P < 0.05, # P < 0.05, $ P < 0.05, & P < 0.05

Article Snippet: KGN cells were treated with 500 nM DHEA for 24 h, followed by removing the medium and replacing medium supplemented with OB (20, 40 and 80 μM) or Colivelin TFA (a STAT3 activator, 0.5 μM, MedChemExpress, USA) for two days [ – ].

Techniques: Western Blot, Expressing, Flow Cytometry

Journal: Frontiers in Immunology

Article Title: Allicin inhibits PD-L1 through the IL-6/JAK2/STAT3 pathway to suppress immune evasion in osteosarcoma

doi: 10.3389/fimmu.2026.1735090

Figure Lengend Snippet: Allicin inhibits the IL-6/JAK2/STAT3 axis in osteosarcoma cells and ultimately suppresses PD-L1 expression. Molecular Docking of Allicin and IL-6 (A) . Western blot analysis of IL-6/JAK2/STAT3 axis protein expression in HOS and K7M2 cell lines (B–E) . Expression levels of phosphorylated STAT3 and PDL1 proteins in HOS cells following Colivelin (phosphorylated STAT3 agonist) treatment (F) . Results are expressed as mean ± SD (***p < 0.001, ****p < 0.0001 vs. the control group).

Article Snippet: Colivelin (STAT3 activator, MedChemExpress, New Jersey, USA) was dissolved in DMSO.

Techniques: Expressing, Western Blot, Control