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

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.

Demonstration of the protective effect of propofol in rat model of cisplatin-induced neuropathy

“…Besides, we demonstrated the positive effects of propofol on antioxidant/oxidant balance with MDA, GSH, TNF-α, IL-6 levels. In various previous studies conducted, it has been shown that propofol prevents apoptosis, has anti-infl ammatory and antioxidant effects and has taken its place in the literature (9)(10)(11)(12)(13)(14)(15)(16)(17)(18). Based on this feature on propofol, we investigated whether it has a curative effect on neurotoxicity by developing a peripheral neurotoxicity model in rats.…”

“…Cisplatin-induced cytotoxicity is caused by oxidative stress, DNA damage, and infl ammatory cytokines [10]. When it comes to neurotoxicity, the pathophysiological mechanisms that contribute to this include infl ammation and oxidative damage as well as DNA damage and apoptotic cell death in the nervous system (11,12).…”

“…Propofol is a fast-acting anesthetic agent administered intravenously. In addition to its anesthetic effects, it has been reported in previous studies that it protects cells and tissues from oxidative stress, reduces apoptosis and infl ammation, and protects against hypoxic/ischemic-induced neuronal damage (9)(10)(11)(12)(13). In a study conducted on rats with traumatic brain injury in the literature, the neuroprotective and anti-infl ammatory effects of propofol were emphasized (14).…”

TMAO promotes NLRP3 inflammasome activation via the ERS/NF-kb pathway in ox-LDL-induced THP-1 macrophages and accelerates the secretion of IL-1β、IL-18

“…Studies has reported that NLRP3 can be activated through multiple pathways including NF-kb [23] ERS [24] ROS [25]and MAPK[26]. Among them, NF-KB has been widely recognized as the canonical pathway of NLRP3 activation.…”

Vascular Repair by Grafting Based on Magnetic Nanoparticles

“…Atherosclerosis (AS) is also a severe disease that can cause vascular damage [ 120 , 121 ]. Although many drugs can treat atherosclerosis [ 122 , 123 , 124 ], their systemic administration has serious disadvantages. In particular, the proportion of therapeutic dose reaching atherosclerotic lesions is small, resulting in poor therapeutic effect.…”