Propofol elicits autophagy via endoplasmic reticulum stress and calcium exchange in C2C12 myoblast cell line

Abstract

In this study, we investigated the relationship between propofol and autophagy and examined whether this relationship depends on ER stress, production of ROS (reactive oxygen species), and disruption of calcium (Ca2+) homeostasis. To this end, we measured C2C12 cell apoptosis in vitro, along with Ca2+ levels; ROS production; and expression of proteins and genes associated with autophagy, Ca2+ homeostasis, and ER stress, including LC3 (microtubule-associate protein 1 light chain 3), p62, AMPK (adenosine 5’-monophosphate (AMP)-activated protein kinase), phosphorylated AMPK, mTOR (the mammalian target of rapamycin), phosphorylated mTOR, CHOP (C/BEP homologous protein), and Grp78/Bip (78 kDa glucose-regulated protein). We found that propofol treatment induced autophagy, ER stress, and Ca2+ release. The ratio of phosphorylated AMPK to AMPK increased, whereas the ratio of phosphorylated mTOR to mTOR decreased. Collectively, the data suggested that propofol induced autophagy in vitro through ER stress, resulting in elevated ROS and Ca2+. Additionally, co-administration of an ER stress inhibitor blunted the effect of propofol.

An integrated characterization of contractile, electrophysiological, and structural cardiotoxicity of Sophora tonkinensis Gapnep. in human pluripotent stem cell-derived cardiomyocytes

“…Besides, the generation of intracellular ROS could induce oxidative damage, and DCFH-DA is generally used to measure ROS generation in cells [24]. The fluorescence images showed that there was a visible increase of the fluorescence staining of ROS (green) in the CMs after treating the high dose of four compounds, the same as statistical results of fluorescence density as shown in Fig.…”

Molecular subtypes of colorectal cancer: An emerging therapeutic opportunity for personalized medicine

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The effect of equipotent dose of propofol and sevoflurane on endoplasmic reticulum stress during breast cancer surgery

“…Propofol exerts an organ protective effect by modulating ER stress, although patterns of ER stress changes vary. Chen et al [ 18 ] revealed that propofol enhanced ER stress and ultimately induced cell apoptosis of unnecessary muscle tissue to protect muscle. By contrast, Wang et al [ 19 ] observed a neuroprotective effect of propofol through a reduction of ER stress and amelioration of neuronal cell apoptosis.…”