Sevoflurane preconditioning at 1.5% significantly restored cardiomyocyte viability and reduced myocardial injury markers cTnI and LDH compared to hypoxia/reoxygenation alone in neonatal rat cardiomyocytes in vitro.
Does sevoflurane preconditioning reduce hypoxia/reoxygenation-induced myocardial injury in neonatal rat cardiomyocytes?
Sevoflurane preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury by modulating the miR-208a-3p/STC1 axis, offering a potential molecular target for myocardial protection.
Effect estimate: Sevoflurane increased cell viability concentration-dependently with 1.5% almost restoring viability to control levels (p<0.0001); reduced myocardial injury markers cTnI and LDH levels significantly (p<0.0001)
p-value: p=<0.0001
Abstract Objectives Myocardial hypoxia/reoxygenation (H/R) injury is a common pathological process in cardiovascular diseases. This study investigates whether sevoflurane alleviates H/R-induced myocardial injury by regulating miR-208a-3p and reveals the underlying molecular mechanisms. The findings may provide new therapeutic strategies for myocardial protection. Methods This study used neonatal rat cardiomyocytes as a model with 6-hour hypoxia treatment to simulate myocardial hypoxia. Cell viability was measured by CCK-8 assay, and miR-208a-3p expression levels were assessed by qRT-PCR. Inflammatory markers, myocardial injury markers, and oxidative stress markers were quantified by ELISA. The interaction between miR-208a-3p and its target gene was confirmed through dual-luciferase assays. Finally, the effects of sevoflurane and H/R treatment on the target gene were examined. Results This experiment found that the expression of miR-208a-3p reached its peak at 6 h of hypoxia. Sevoflurane preconditioning can concentration-dependently enhance cell viability, inhibit the upregulation of miR-208a-3p, and reduce the levels of myocardial injury markers cTnI and LDH. However, overexpression of miR-208a-3p inhibited cell activity, increased the levels of inflammatory, and promoted inflammatory responses. Meanwhile, overexpression of miR-208a-3p decreased SOD activity, increased MDA levels, and significantly enhanced oxidative stress. Mechanistically, sevoflurane enhances myocardial protection by targeting the 3′UTR of STC1 and upregulating STC1 expression. Conclusions Sevoflurane significantly alleviates H/R-induced myocardial injury by modulating miR-208a-3p, and this finding provides a new molecular target and potential therapeutic strategy for myocardial protection.
Sun et al. (Thu,) conducted a other in Neonatal rat cardiomyocytes subjected to hypoxia/reoxygenation-induced myocardial injury in vitro. Sevoflurane preconditioning vs. Hypoxia/reoxygenation without sevoflurane preconditioning was evaluated on Cell viability and myocardial injury markers (cTnI, LDH) after hypoxia/reoxygenation injury (Sevoflurane increased cell viability concentration-dependently with 1.5% almost restoring viability to control levels (p<0.0001); reduced myocardial injury markers cTnI and LDH levels significantly (p<0.0001), p=<0.0001). Sevoflurane preconditioning at 1.5% significantly restored cardiomyocyte viability and reduced myocardial injury markers cTnI and LDH compared to hypoxia/reoxygenation alone in neonatal rat cardiomyocytes in vitro.