Peroxynitrite Mediates Diabetes-Induced Endothelial Dysfunction: Possible Role of Rho Kinase Activation
Figure 4
FeTPPs inhibited diabetes-induced RhoA activation in rat vessels and BAEC. (a) Pull-down assay showed significant increases in active RhoA in diabetic aortic homogenate compared to that of controls that were blocked by cotreatment with FeTPPs (). Values are expressed as means ± SEM, versus control. (b) Bovine aortic endothelial cells (BAECs) were incubated with normal (NG, 5 mM) and high glucose (HG, 25 mM) for 3 days or exogenous peroxynitrite (PN, 100 M) for 18 hours (n = 4 in each group). High glucose significantly increased active RhoA, which was prevented by cotreatment with FeTPPs (Fe, 2.5 M). Peroxynitrite exerted similar effects to high-glucose in increasing active RhoA (~2-fold) compared to decomposed peroxynitrite (DPN). Values are expressed as means ± SEM, versus control.
