Propofol alleviates inflammation and apoptosis in HCY-induced HUVECs by inhibiting endoplasmic reticulum stress

Atherosclerosis is a chronic vascular inflammatory disease, and is associated with oxidative stress and endothelial dysfunction. Homocysteine (HCY) can cause damage to endothelial cells via the enhancement of the endoplasmic reticulum stress (ERS) pathway. Propofol has a protective effect on endothelial injury and can suppress inflammation and oxidation. The purpose of the present study was to investigate the protective effect of propofol on HCY-induced inflammation and apoptosis of human umbilical vein endothelial cells (HUVECs). HCY was used to establish the endothelial injury model. Cell Counting Kit-8 assays and flow cytometry were used to detect cell viability and apoptosis, respectively. Then, ELISA was performed to examine the expression levels of inflammatory cytokines, and the expression levels of proteins related to inflammation, apoptosis and ERS were determined via western blotting. Results showed that propofol increased cell viability, suppressed NF-kappa B signaling pathway activation and decreased the expression levels of inflammatory factors in HUVECs induced by HCY. Moreover, propofol could inhibit the expression of proteins involved in ERS, including ER chaperone BiP (Bip), C/EBP-homologous protein, protein kinase R-like ER kinase and inositol-requiring 1 alpha, and reduce cell apoptosis of HCY-induced HUVECs. However, the overexpression of Bip could reactivate ERS and the NF-kappa B signaling pathway, as well as promote inflammation and cell apoptosis, when compared with HCY-treated groups. In conclusion, propofol can ameliorate inflammation and cell apoptosis of HUVECs induced by HCY via inhibiting ERS, which may provide a novel insight into the treatment of atherosclerosis.

Automated summary

The study demonstrated that propofol protects against inflammation and cell apoptosis in HUVECs induced by HCY by inhibiting endoplasmic reticulum stress (ERS), providing a potential therapeutic strategy for atherosclerosis.