Abstract
ABSTRACTSevoflurane (Sev) has a cardioprotective role in myocardial ischemia/reperfusion injury (MI/RI), but its mechanism has not been fully elucidated. This study aimed to investigate whether the circ_CDR1as/miR‐671‐5p/HMGA1 axis mediates the cardioprotective effect of Sev in MI/RI. Cardiomyocytes underwent hypoxia/reoxygenation (H/R) treatment was used to simulate MI/RI in vitro. H/R cardiomyocytes were then pretreated with Sev to explore the protective effect of Sev on H/R cells. The level of CDR1as/miR‐671‐5p/HMGA1 axis were detected by RT‐qPCR. The proliferation and apoptosis of cardiomyocytes were detected by CCK‐8 and flow cytometry. The levels of myocardial injury markers and inflammatory markers were detected by ELISA assay. Finally, the regulatory relationship between CDR1as and miR‐671‐5p/HMGA1 axis was verified by Dual‐luciferase reporting and RNA pull‐down assays. Sev Pretreatment can reduce the level of CDR1as and mitigate H/R‐induced damage to cardiomyocytes. This Pretreatment lowers the levels of myocardial injury markers, oxidative stress markers, and pro‐inflammatory factors in H/R‐affected cardiomyocytes. However, CDR1as overexpression inhibits Sev's protective effect on H/R cardiomyocytes. At the molecular mechanism, we found that CDR1as mediates Sev's protective effect through the CDR1as/miR‐671‐5p/HMGA1 axis. CDR1as increases HMGA1 levels by sponging miR‐671‐5p, while high HMGA1 levels diminish Sev's protective effect. Sev plays a cardioprotective role in MI/RI by inhibiting the circ_CDR1as/miR‐671‐5p/HMGA1 axis.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call