Dexmedetomidine attenuates myocardial ischemia–reperfusion injury in hyperlipidemic rats by inhibiting inflammation, oxidative stress and NF‐κB

The present study was conducted to determine the protective effect of Dexmedetomidine (DEX) in myocardial ischemia-reperfusion injury in hyperlipidemic rats. Towards this, the effect of DEX was first evaluated on the infarct size and the histopathology of cardiac tissues using TTC and H and E staining, and it was found that DEX significantly improved the infarct size and architecture of the myocardial tissues following the I/R injury. DEX also showed significant improvement in various examined hemodynamic parameters (e.g., LVSP, and ± dp/dtmax ) in a dose-dependent manner. The lipid profile (LDL, VLDL, TC, TG, and HDL level) of the rats were also found significantly improved in DEX-treated rats. The level of various pro-inflammatory cytokines (IL-1β, IL-6, IL-10, IL-17, and TNF-α), cardiac injury (CK, CK-MB, Troponin I AST, ALT, and LDH), and oxidative stress (MDA, SOD, and GSH) biomarkers were also found to be restored near to the normal in DEX-treated group. It has been found that DEX also significantly reduces apoptosis of rat cardiomyocytes. In western blot analysis, DEX showed a significant reduction in the activation of NF-κB. In conclusion, our study demonstrated the protective effect of Dexmedetomidine in myocardial ischemia-reperfusion injury in hyperlipidemic rats possibly via amelioration of oxidative stress, and inflammation apoptosis.