Homocysteine Induces Apoptosis of Human Umbilical Vein Endothelial Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

Figure 5

NOX4 inhibition alleviated mitochondrial dysfunction, suppressed the activation of ER stress and NF-κb, and decreased apoptosis induced by Hcy in HUVEC. (a, b, c) The expression levels of NOX4, cytoplasmic cytochrome c, cleaved caspase-3, and procaspase-3 were determined via Western blot analysis. β-actin was selected as the loading control. (d, e, f, g) The expression of GRP78, p-eIF2a and eIF2a, ATF4, and CHOP was determined via Western blot analysis. β-actin was selected as the loading control. (h) The production of mitochondrial ROS was detected in different treatments groups. (j) The apoptotic rates of HUVEC exposed to different treatments were evaluated. The data are presented as the means ± SD of three independent experiments. versus the control group; ^#, ^## versus the Hcy group.

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