Sirt1 Protects Endothelial Cells against LPS-Induced Barrier Dysfunction

Figure 7

Effect of Sirt1 on the alteration of protein expression and activity of SOD2, as well as on NOX4 generation in HUVECs. (a) LPS evoked the decline in SOD2 expression in a time-dependent manner. (b) LPS induced tyrosine nitration of SOD2. (c–e) SRT1720 abolished the decrease in SOD2 expression upon LPS stimulation while ex527, as well as Sirt1 siRNA, duplicated the effect. (f) The Sirt1 activator reversed the LPS-induced decrease in SOD activity. ECs were treated with or without SRT1720 or ex527, followed by treatment of LPS (500 ng/mL, 1 h); then, SOD activity was detected using an SOD assay kit. (g) The NOX4 inhibitor apocynin (300 μmol/L, 1 h) attenuated LPS-induced ROS generation. ROS was measured through a fluorescent microscope. (h) SRT1720 abolished LPS-induced NOX4 elevation. . versus control or control siRNA, ^# versus LPS or control siRNA + LPS.

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