Sevoflurane preconditioning attenuates myocardial cell damage caused by hypoxia and reoxygenation via regulating...

Myocardial ischemia-reperfusion (I/R) injury is the leading reason for perioperative adverse cardiac incidents and mortality. Sevoflurane (Sevo) has an essential role in the management of myocardial I/R injury. The aim of this research was to explore whether miR-92a-3p mediated the influences of Sevo on myocardial cell damage by constructing a hypoxia and reoxygenation (H/R) model to simulate I/R.

H/R models were established in vitro, preconditioned with Sevo and further transfected with miR-92a-3p mimic. RT-qPCR was used to examine miR-92a-3p expression. Cell viability and apoptosis were measured by MTT assay and flow cytometry. Levels of myocardial injury-related markers cTnI, CK-MB, and LDH detected by ELISA. Interaction of miR-92a-3p with UGP2 was tested by luciferase reporter gene assay.

H/R treatment resulted in significantly higher miR-92a-3p expression in H9c2 cells than the control group, while Sevo treatment reduced miR-92a-3p expression. H/R treatment resulted in decreased cell viability, enhanced apoptosis, as well as elevated cTnI, CK-MB, and LDH levels, whereas Sevo treatment reversed these trends. Transfection of miR-92a-3p mimic under Sevo treatment counteracted the effect of Sevo on H9c2 cell viability, apoptosis, cTnI, CK-MB and LDH. Additionally, we identified UGP2 as a target gene of miR-92a-3p.

Sevo reversed H/R-induced myocardial cell damage in a model of H/R in vitro. Sevo preconditioning modulates H/R-induced myocardial cell damage by negatively mediating miR-92a-3p levels.