Sevoflurane preconditioning improved cell viability and reduced apoptosis in hypoxia/reoxygenation-injured cardiomyocytes by upregulating miR-451a to suppress IL6R expression (p < 0.001).
Does sevoflurane preconditioning mitigate hypoxia/reoxygenation injury in cardiomyocytes?
Sevoflurane preconditioning protects cardiomyocytes from hypoxia/reoxygenation injury by upregulating miR-451a and suppressing IL6R, highlighting a potential therapeutic mechanism for myocardial ischemia/reperfusion injury.
Absolute Event Rate: 0% vs 0%
ABSTRACT This study investigated whether Sevoflurane preconditioning (Sevo‐pre) attenuates hypoxia/reoxygenation (H/R)‐triggered myocardial damage by targeting microRNA‐451a (miR‐451a) and its downstream target interleukin 6 receptor (IL6R). Rat embryonic cardiomyoblast‐derived H9C2 underwent H/R injury modeling with either Sevo‐pre or no preconditioning. Mechanistic studies employed the manipulation of miR‐451a overexpression and silencing, alongside IL6R modulation via targeted siRNA and plasmid transfection. Sevo‐pre significantly enhanced cell viability, reduced apoptosis, and decreased injury markers in H/R‐induced cells ( p < 0.001). Notably, miR‐451a was downregulated in H/R conditions but upregulated by Sevo‐pre. The inhibition of miR‐451a negated Sevo's protective effects, exacerbating oxidative stress and apoptosis ( p < 0.001). Bioinformatics analyses and luciferase assays identified IL6R as a direct target of miR‐451a. Silencing IL6R mitigated the adverse effects of miR‐451a inhibition, restoring cell viability and reducing oxidative stress ( p < 0.001). Sevo‐pre alleviates H/R injury in cardiomyocytes through the regulation of miR‐451a, which suppresses IL6R expression, consequently reducing oxidative stress and apoptosis. This study elucidates a novel cardioprotective mechanism of preconditioning via the miR‐451a/IL6R axis, which highlights miR‐451a and IL6R as potential therapeutic targets for mitigating myocardial I/R injury in clinical settings.
Li et al. (Thu,) reported a other. Sevoflurane preconditioning improved cell viability and reduced apoptosis in hypoxia/reoxygenation-injured cardiomyocytes by upregulating miR-451a to suppress IL6R expression (p < 0.001).