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.

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 expression 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 protein of hypoxia-induced PC12 cells, while decreased cell apoptosis rate, Cleaved-caspase-3 protein expression and levels of inflammatory 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. [ABSTRACT FROM AUTHOR]