Protective Effect of Isoflurane on Hypoxia/Reoxygenation-Induced Myocardial Injury via miR-548a-5p Regulation of PTEN.

Ischemia-reperfusion (I/R) injury induces cardiomyocyte apoptosis, oxidative stress and elevated myocardial injury markers. This study aimed to investigate whether the microRNA-548a-5p (miR-548a-5p)/phosphatase and tensin homolog deleted on chromosome 10 (PTEN) axis mediates the cardioprotection conferred by isoflurane (ISO). An in vitro hypoxia/reoxygenation (H/R) injury model was established using H9c2 cardiomyocytes, including control, H/R and ISO pretreatment groups. We detected miR-548a-5p and PTEN expression by RT-qPCR, and evaluated cell viability, apoptosis, myocardial injury markers including creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), lactate dehydrogenase (LDH), and reactive oxygen species (ROS) using CCK-8, flow cytometry, ELISA and DCFH-DA staining. Dual-luciferase reporter assay validated the direct binding between miR-548a-5p and PTEN. H/R downregulated miR-548a-5p and upregulated PTEN, accompanied by decreased cell viability, increased apoptosis, myocardial injury and oxidative stress. 1.0% ISO pretreatment reversed these adverse alterations, restored miR-548a-5p and suppressed PTEN expression. miR-548a-5p inhibition attenuated ISO-elicited cardioprotection, whereas PTEN silencing restored the cardioprotective capacity compromised by miR-548a-5p inhibition. In conclusion, ISO exerts cardioprotective effects via the miR-548a-5p/PTEN signaling axis, offering a potential therapeutic target for I/R injury.