Skip to main content
Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: KLF4 alleviates cerebral vascular injury by ameliorating vascular endothelial inflammation and regulating tight junction protein expression following ischemic stroke

Fig. 7

The 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. ci 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 significant

Back to article page