右美托咪定
氧化应激
心肌保护
再灌注损伤
炎症
医学
缺血
内科学
药理学
免疫印迹
内分泌学
细胞凋亡
化学
生物化学
基因
镇静
作者
Weiwei Gao,Liang Du,Nan Li,Yating Li,Jinfang Wu,Ze Zhang,Huan Chen
摘要
) 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.
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