Abstract

BackgroundIsoflurane can cause hepatotoxicity, and microRNAs (miRNAs) are involved in the regulation of liver injury. Therefore, this study aimed to explore the effect of miR-125a-5p on isoflurane-induced liver injury. Basic proceduresSprague-Dawley (SD) male rats and BRL-3A cells were exposed to isoflurane to construct animal and cell models. Serum alanine transaminase (ALT) and aspartate transaminase (AST) levels of rats were detected. RT-qPCR was performed for the measurement of miR-125a-5p levels. Cell proliferation and apoptosis were also detected. Main findingsAfter isoflurane treatment, serum ALT and AST levels of rats increased in a time-dependent manner, and the differences reached significant levels from 3 days after isoflurane treatment. MiR-125a-5p levels increased significantly in the liver tissues of isoflurane-treated rats. MiR-125a-5p downregulation significantly attenuated isoflurane-induced increasing trend of serum ALT and AST levels in rats. In BRL-3A cells, isoflurane treatment significantly inhibited cell proliferation and promoted cell apoptosis, which was reversed by miR-125a-5p downregulation. Principal conclusionsIsoflurane exposure significantly elevates the level of miR-125a-5p in the liver tissues of rats. Downregulation of miR-125a-5p may protect against isoflurane-induced liver injury through regulating liver cell proliferation and apoptosis. Dysregulation of miR-125a-5p might be a possible mechanism of isoflurane-induced liver injury.

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