Abstract
This study is to investigate the effects of dexmedetomidine on myocardial ischemia-reperfusion (I/R) injury and its molecular mechanisms. H9c2 cell injury model was constructed by the hypoxia/normoxia (H/R) conditions. Besides, cAMP response element-binding protein (CREB) overexpression and knockdown cell lines were constructed. Cell viability was determined by cell-counting kit 8. Biochemical assays were used to detect oxidative stress-related biomarkers, cell apoptosis, and ferroptosis-related markers. Our results showed that dexmedetomidine's protective effects on H/R-induced cell damage were reversed by the inhibition of protein kinase A (PKA), CREB, and extracellular signal regulated kinase 1/2 (ERK1/2). Treatment of dexmedetomidine ameliorated oxidative stress in the cardiomyocytes induced by H/R, whereas inhibition of PKA, CREB, or ERK1/2 reversed these protective effects. Cell death including cell necrosis, apoptosis, and ferroptosis was found in the cells under H/R insult. Interestingly, targeting CREB ameliorated ferroptosis and oxidative stress in these cells. In conclusion, dexmedetomidine attenuates myocardial I/R injury by suppressing ferroptosis through the cAMP/PKA/CREB signaling pathway.
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