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Protocatechuic Aldehyde Inhibits Lipopolysaccharide‐induced Human Umbilical Vein Endothelial Cell Apoptosis via Regulation of Caspase‐3

Apoptosis of vascular endothelial cells results in the loss of endothelial integrity, and is a risk factor of atherosclerosis (AS). Lipopolysaccharide (LPS) stimulates inflammation during AS. The current study examined the effect of a potent water‐soluble antioxidant, protocatechuic aldehyde (PCA; derived from the Chinese herb Salvia miltiorrhiza) on apoptosis in human umbilical vein endothelial cells (HUVECs) stimulated with LPS. The LPS (15 µg/ml) stimulation for 30 h resulted in significant HUVEC apoptosis, as detected by Hoechst 33258 staining and Annexin V analysis. The PCA (0.25–1.0 mmol/L, 12 h) inhibited LPS‐induced HUVEC apoptosis in a dose‐dependent manner. Lipopolysaccharide induced caspase‐3 activation, but had no significant effect on caspase‐2, Bcl‐2/Bax, cytochrome c, caspase‐9 and granzyme B expression. Protocatechuic aldehyde (0.25–1.0 mmol/L) significantly inhibited caspase‐3 activation in a dose‐dependent manner. A specific caspase‐3 inhibitor also protected against LPS‐induced apoptosis; however, no cooperative effect of PCA and the inhibitor was observed in this study. Collectively, these results indicate that PCA inhibits LPS‐induced apoptosis in HUVECs through a mechanism that involves caspase‐3. Copyright © 2012 John Wiley & Sons, Ltd.