Fig. 7From: KLF4 alleviates cerebral vascular injury by ameliorating vascular endothelial inflammation and regulating tight junction protein expression following ischemic strokeThe effect of overexpression of KLF4 on the expression of three cell adhesion molecules, phosphorylated NF-κB, and tight junction proteins in bEnd3 cells under OGD/R conditions. a Representative images of western blot for the expression of KLF4 in the bEnd3 cells in the control plasmid (mock) or KLF4 overexpression group. b Representative images of western blot for the expression of KLF4, E-selectin, VCAM-1, ICAM-1, p-NF-κB, Claudin-5, and ZO-1 in the bEnd3 cells of mock and KLF4 overexpression group at 12 h restoration of OGD or NO-OGD/R. c–i Densitometric analysis shows the ratios of KLF4/β-actin (c), E-selectin/β-actin (d), VCAM-1/β-actin (e), ICAM-1/β-actin (f), phosphorylated NF-κB/total NF-κB (g), Claudin-5/β-actin (h), and ZO-1/β-actin (i). NO-OGD/R mock-treated cells served as control. Data represent mean ± standard deviation and were analyzed by two-way ANOVA (n = 5 per experimental group). Note that the expressions of three cell adhesion molecules including E-selectin, VCAM-1, and ICAM-1 and the phosphorylation of NF-κB on mock-treated bEnd3 cells were significantly induced in response to OGD/R, but the expression of Claudin-5 and ZO-1 markedly decreased compared to that of the NO-OGD/R mock-treated controls. However, these effects were significantly rescued by overexpressing the levels of KLF4 in the bEnd3 cells. *P < 0.05, **P < 0.01, ***P < 0.001; ns, not significantBack to article page