Etomidate Regulates miR-192-5p Expression to Reduce Hypoxia-Reoxygenation Induced Bronchial Epithelial Cell Damage

Abstract

Etomidate is a new type of intravenous anesthetic that can protect bronchial epithelial cells from oxidative stress damage. miR-192-5p is upregulated in 6-hydroxydopamine-induced neurocytes. This study explored the effect of etomidate on bronchial epithelial cell apoptosis and oxidative stress induced by hypoxia and reoxygenation and its regulatory effect on miR-192-5p. The human bronchial epithelial cells BEAS-2B were cultured in vitro and then subjected to hypoxia and reoxygenation to establish a cell injury model. The cells were then treated with etomidate at different doses. Moreover, anti-miR-NC and anti-miR-192-5p were transfected into the BEAS-2B cells to treat the hypoxia-reoxygenation. Moreover, miR-NC and miR-192-5p mimics were transfected into BEAS-2B cells, followed by treatment with 90 µmol/L etomidate for 24 h and then treatment with hypoxia and reoxygenation. The 2,4-dinitrophenylhydrazine method was used to determine the level of LDH in the culture medium of cardiomyocytes. Thiobarbituric acid was used to determine the level of MDA and xanthine oxidase to determine the activity of SOD. Flow cytometry was used to measure the apoptosis rate and qRT-PCR to evaluate miR-192-5p expression. Western blotting was used to determine the Bax and Bcl-2 protein levels. Compared with the findings in the control group, the levels of LDH and MDA, the apoptosis rate, and the protein level of Bax were increased (P < 0.05) upon treatment with hypoxia and reoxygenation, while SOD activity and Bcl-2 protein level were decreased (P < 0.05). In a manner dependent on the dose, etomidate could significantly reverse the effects of hypoxia and reoxygenation on oxidative stress and apoptosis of BEAS-2B cells (P < 0.05). Hypoxia and reoxygenation could significantly increase the miR-192-5p level of BEAS-2B cells (P < 0.05), while etomidate could reduce this miR-192-5p expression (P < 0.05) in a dose-dependent manner. Transfection of anti-miR-192-5p dramatically reduced LDH, MDA, apoptosis rate, and Bax protein level (P < 0.05), but was associated with increases of SOD activity and Bcl-2 protein expression (P < 0.05). High expression of miR-192-5p could significantly reverse the influence of etomidate on apoptosis and oxidative stress of BEAS-2B cells induced by hypoxia-reoxygenation (P < 0.05). Etomidate restrained the apoptosis of bronchial epithelial cells and oxidative stress induced by hypoxia and reoxygenation by inhibiting miR-192-5p expression, thereby reducing cell damage.