Ligustrazine Protects Homocysteine-Induced Apoptosis in Human Umbilical Vein Endothelial Cells by Modulating Mitochondrial Dysfunction.

Ligustrazine is one of the alkaloid compounds isolated from the traditional Chinese herb, which shows protective effects on cardiovascular disorders. High homocysteine (Hcy) level can predict cardiovascular-related events including death. In this study, we used Hcy to stimulate the human umbilical vein endothelial cells (HUVECs) and investigated the protective effect of ligustrazine on endothelial dysfunction by assessing the cell apoptosis, oxidative damage, mitochondrial dysfunction, and the potential molecular pathways. Our results clearly showed that ligustrazine increased HUVEC cell viability, decreased the dehydrogenase (LDH) level, and inhibited HUVEC apoptosis, which was associated with the attenuation of attenuated oxidative damage. The mitochondrial-dependent pathway was closely related in the regulation of ligustrazine, reflected by the attenuated mitochondrial membrane potential change and decreased cytochrome c release from the mitochondria to the cytosol. Ligustrazine may protect Hcy-induced apoptosis in HUVECs by attenuating oxidative damage and modulating mitochondrial dysfunction.