Fig. 7: BP-1-102 inhibited AngII-induced JAK2/STAT3 and NF-kB signaling activation in VSMCs. | Cell Death & Disease

Fig. 7: BP-1-102 inhibited AngII-induced JAK2/STAT3 and NF-kB signaling activation in VSMCs.

From: A novel STAT3 inhibitor attenuates angiotensin II-induced abdominal aortic aneurysm progression in mice through modulating vascular inflammation and autophagy

Fig. 7

a VSMCs were treated with AngII (10 μM) for 24 and 48 h. JAK2/STAT3 and NF-kB signaling pathway related proteins expression were evaluated and compared with untreated VSMCs. VSMCs were treated with BP-1-102 (0.01–0.5 μM) for 24 h. JAK2/STAT3 and NF-kB signaling pathway related proteins expression were evaluated. VSMCs were treated with AngII (10 μM) + BP-1-102 (0.01–0.5 μM) for 24 h. b Relative protein levels of were determined by normalized with β-actin expression in BP-1-102 (0.01–0.5 μM) groups, respectively, and compared with untreated VSMCs (mock) or with BP-1-102 (0.01 μM) group. The results were presented as mean ± standard deviation (SD). n= 4, *P < 0.01 compared with Mock. NS indicates non-significant differences compared with Mock. #P < 0.01 compared with BP-1-102 (0.01 μM) group (two-way ANOVA followed by Tukey’s test). c Relative protein levels were determined by normalized with β-actin expression in AngII (10 μM) (24 or 48 h) groups, AngII (10 μM) + BP-1-102 (0.01–0.5 μM) groups, respectively, and compared with untreated VSMCs (mock) or with AngII (10 μM) for 24 h group. The results were presented as mean ± standard deviation (SD). n= 4, *P < 0.01 compared with Mock. #P < 0.01 compared with AngII (10 μM) 24 h group. NS indicates non-significant differences compared with AngII (10 μM) 24 h group (two-way ANOVA followed by Tukey’s test).

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