Abstract
Isoflurane has been studied in ischemia-reperfusion injury, while the regulatory mechanism by which isoflurane regulates microRNA(miR)-9-3p in hepatic ischemia/reperfusion injury (HIRI) via targeting fibronectin type III domain containing 3B (FNDC3B) remains seldom investigated. This study aims to determine the role of miR-9-3p in HIRI progression under the treatment of isoflurane. Rat HIRI models were established and treated with isoflurane. MiR-9-3p was altered to assess its role in inflammation, oxidative stress, transaminases, pathology, and hepatocyte apoptosis in HIRI rat liver tissues. Expression of miR-9-3p and FNDC3B in rat liver tissues was determined, and the targeting relationship between miR-9-3p and FNDC3B was confirmed using bioinformatic prediction and dual luciferase reporter gene assay. MiR-9-3p was downregulated, whereas FNDC3B was upregulated in HIRI rat liver tissues. Isoflurane treatment upregulated miR-9-3p and attenuated pathological changes, inflammation, oxidative stress, transaminases, and hepatocyte apoptosis in HIRI rat liver tissues. MiR-9-3p upregulation further strengthened the effect of isoflurane on HIRI, while miR-9-3p downregulation suppressed the therapeutic role of isoflurane. FNDC3B was confirmed as a target gene of miR-9-3p. Isoflurane upregulates miR-9-3p to protect rats from HIRI by inhibiting FNDC3VB. Our research may provide novel targets for HIRI treatment.