Department of Pharmacodynamics and Toxicology, School of Pharmacy, Zabol University of Medical Sciences, Zabol, Iran; Students Research Committee, School of Pharmacy, Zabol University of Medical Sciences, Zabol, Iran.
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Zabol University of Medical Sciences, Zabol, Iran.
Environ Toxicol Pharmacol. 2016 Sep;46:110-115. doi: 10.1016/j.etap.2016.07.010. Epub 2016 Jul 19.
Carbon monoxide (CO) poisoning leads to tissue hypoxia resulting in cardiovascular disturbances. Resveratrol (RES) is considered a natural cardioprotective agent especially in the setting of ischemia/reperfusion injury. In the present study, the cardioprotective potential of RES against CO-induced cardiotoxicity was evaluated. 45 male Wistar rats, animals were randomly assigned to 5 experimental groups. The first group served as negative control and was not exposed to CO. All remaining rats were exposed to CO 3000ppm for 60min. The second group received normal saline following CO exposure, while groups 3, 4 and 5 were injected intraperitoneally with different doses of RES (1, 5 and 10mg/kg, respectively). Histopathological examination showed that RES administration reduced myocardial lesions compared to control groups. Myocardial Akt expression was significantly increased in rats treated with the highest dose of RES (p<0.05) compared to CO-exposed non-treated animals. Caspase-3 activity in rat cardiomyocytes of RES-treated animals was significantly decreased in a dose-dependent manner. ECG findings did not differ significantly among CO-exposed groups. In conclusion, the present study offers evidence of a protective effect of RES administration on CO-induced cardiotoxicity via Akt up-regulation and attenuation of caspase-3 activity in rat hearts.
一氧化碳（CO）中毒会导致组织缺氧，从而引起心血管紊乱。白藜芦醇（RES）被认为是一种天然的心脏保护剂，特别是在缺血/再灌注损伤的情况下。在本研究中，评估了 RES 对 CO 诱导的心脏毒性的心脏保护作用。45 只雄性 Wistar 大鼠，动物被随机分配到 5 个实验组。第一组作为阴性对照，不接触 CO。其余所有大鼠均暴露于 3000ppm CO 中 60 分钟。第二组在 CO 暴露后接受生理盐水，而第 3、4 和 5 组分别腹腔注射不同剂量的 RES（1、5 和 10mg/kg）。组织病理学检查显示，与对照组相比，RES 给药减少了心肌损伤。与 CO 暴露未治疗的动物相比，用 RES 处理的大鼠心肌中的 Akt 表达明显增加（p<0.05）。RES 处理动物的心肌细胞中 caspase-3 活性呈剂量依赖性显著降低。ECG 结果在 CO 暴露组之间没有显著差异。总之，本研究提供了证据，证明 RES 给药通过上调 Akt 和抑制 caspase-3 活性对 CO 诱导的心脏毒性具有保护作用。
