依托咪酯通过促进miR-142-3p表达减轻缺氧诱导的PC12细胞神经炎症反应和细胞凋亡的分子机制研究OACSCDCSTPCD

Objective:To investigate whether etomidate affects inflammatory response and apoptosis of PC12 cells induced by hypoxia by regulating miR-142-3p.Methods:PC12 cells were pretreated with different doses(2,6,12 µmol/L)of etomidate to establish hypoxia model;PC12 cells that transfected with miR-142-3p mimics or inhibitors were pretreated with 0 or 12 µmol/L of etomidate to establish hypoxia model.Cell viability,apoptosis and protein(CyclinD1,Cleaved-caspase-3)expressions were detected by CCK-8 method,flow cytometry and Western blot,respectively.ELISA was used to detect levels of inflammatory factors TNF-α,IL-1β,IL-6.Expression of miR-142-3p was detected by RT-qPCR.Results:Etomidate increased hypoxia-induced PC12 cells activity and expres-sion of CyclinD1 protein and miR-142-3p,while decreased cell apoptosis rate,Cleaved-caspase-3 protein expression and levels of inflammatory factors TNF-α,IL-1β,IL-6(P<0.05).Up-regulation of miR-142-3p increased activity and expression of CyclinD1 pro-tein of hypoxia-induced PC12 cells,while decreased cell apoptosis rate,Cleaved-caspase-3 protein expression and levels of inflamma-tory factors TNF-α,IL-1β,IL-6(P<0.05).Down-regulation of miR-142-3p reversed effects of etomidate on hypoxia-induced PC12 cell activity,apoptosis and expressions of inflammatory factors(P<0.05).Conclusion:Etomidate can reduce inflammatory response and apoptosis of PC12 cells induced by hypoxia,and its mechanism may be related to the up-regulation of miR-142-3p expression in cells.