Open AccessPropofol alleviates inflammation and apoptosis in HCY‑induced HUVECs by inhibiting endoplasmic reticulum stress
Author(s) -
Cunliang Ji,
Yi Hu,
Jing Huang,
Wenzhong Zhang,
Mingfeng Zheng
Publication year - 2021
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2021.11972
Subject(s) - unfolded protein response , inflammation , apoptosis , endoplasmic reticulum , microbiology and biotechnology , oxidative stress , viability assay , signal transduction , endothelial stem cell , biology , pharmacology , chemistry , cancer research , immunology , biochemistry , in vitro
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‑κB 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 1α, and reduce cell apoptosis of HCY‑induced HUVECs. However, the overexpression of Bip could reactivate ERS and the NF‑κB 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.