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

Ji,Cunliang; Yi,Hu; Huang,Jing; Zhang,Wenzhong; Zheng,Mingzhi

doi:10.3892/mmr.2021.11972

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

Authors:
- Cunliang Ji
- Hu Yi
- Jing Huang
- Wenzhong Zhang
- Mingzhi Zheng
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Affiliations: Department of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, P.R. China, Department of Anesthesiology, The Affiliated Zhuzhou Hospital of Xiangya School of Medicine CSU, Zhuzhou Central Hospital, Zhuzhou, Hunan 412000, P.R. China, School of Safety Engineering, North China Institute of Science and Technology, Langfang, Hebei 065201, P.R. China
Published online on: March 8, 2021 https://doi.org/10.3892/mmr.2021.11972
Article Number: 333
Copyright: © Ji et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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.

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