S100A8 Promotes ox-LDL-Induced Oxidative Damage of Vascular Endothelial Cells

The aim of this study was to investigate the physiological function and mechanism of S100A8 protein in ox-LDL-induced oxidative damage of vascular endothelial cells. ox-LDL induced HUVEC oxidative damage model was established in vitro, and the expression level of S100A8 was detected by real-time qPCR and Western blot. The expression of S100A8 was knocked down by transfection of control siRNA and S100A8 siRNAs. The cells viability was detected by CCK-8 assay, the endothelial activation was evaluated though the expression of ICAM-1, VCAM-1 and E-Selectin, which were measured by real-time qPCR assay, and the apoptotic rate and mitochondrial ROS accumulation level were detected by flow cytometry. In order to clarify the mechanism of S100A8 promoting ox-LDL-induced cellular oxidative damage, the effect of S100A8 knockdown on SIRT6 expression level was analyzed by Western blot, and the cells viability and mitochondrial ROS accumulation were detected in SIRT6 knockdown cells. The results showed that the expression level of S100A8 in vascular endothelial cells was up-regulated in ox-LDL-induced oxidative damage. S100A8 knockdown significantly inhibited ox-LDL-induced oxidative damage, apoptosis and mitochondrial reactive oxygen species accumulation. Knockdown of S100A8 increased SIRT6 expression. Simultaneous knockdown of S100A8 and SIRT6 in cells could not inhibit ox-LDL-induced oxidative damage. In conclusion, this study found that in ox-LDL-induced cellular oxidative damage, the expression level of S100A8 was up-regulated, and by inhibiting the expression of SIRT6, the accumulation of mitochondrial reactive oxygen species was promoted, leading to cell apoptosis.

CSTR: 32200.14.cjcb.2023.04.0004