Role of endoplasmic reticulum stress in ketamine-induced apoptosis in rat neurons: an in vitro experiment / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the role of endoplasmic reticulum stress in ketamine-induced apoptosis in rat neurons.Methods Rat adrenal pheochromocytoma cell line (PC12 cells) was seeded in the culture dishes 100 mm in diameter (10 ml/dish) or in 6-well plates (2 ml/well) at a density of 5 × 105 cells/ml.PC12 cells were divided into 4 groups (n =6 each) using a random number tablecontrol group (group C);ketamine group (group K);endoplasmic reticulum stress inhibitor salubrinal group (group S);ketamine + salubrinal group (group K+S).In group C,the cells were cultured in the plain culture medium.In group K,1.5 mmol/L ketamine was added.In group S,30 mmol/L salubrinal was added.In group K + S,1.5 mmol/L ketamine and 30 mmol/L salubrinal were added.At 24 h of incubation,the cell morphology was observed under light microscope,the expression of Bip and caspase-12 in PC12 cells was detected by Western blot,and the cell apoptosis was measured by flow cytometry.The apoptosis rate was calculated.Results Compared with group C,the expression of Bip and caspase-12 was significantly upregulated,and the apoptosis rate was increased in K and K + S groups (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group S (P＞ 0.05).Compared with group K,the expression of Bip and caspase-12 was significantly down-regulated,and the apoptosis rate was decreased in group K+S (P＜0.05).The degree of damage to PC12 cells was more serious in group K than in group C..The degree of damage to PC12 cells in group K+S was significantly mnilder than that in group K and more serious than that in group C.Conclusion The mechanism by which ketamine induces neuronal apoptosis is related to the enhancement of endoplasmic reticulum stress in rats.