蒿甲醚通过调节氧化应激改善阿霉素诱导小鼠心肌损伤的作用研究

Artemether Ameliorates Adriamycin-induced Myocardial Injury in Mice by Modulating Oxidative Stress

目的探讨蒿甲醚对阿霉素诱导的小鼠心肌损伤的保护作用。方法将雄性BALB/c小鼠随机分为正常组、模型组、蒿甲醚组(3 g·kg^(-1)),每组6只。采用阿霉素诱导心肌损伤小鼠模型。测定各组小鼠体质量及心脏质量;检测血清乳酸脱氢酶(LDH)和肌酸激酶(CK)水平;采用苏木精-伊红(HE)染色法观察小鼠心脏组织病理变化;采用Western Blot法及免疫组化法检测各组小鼠心脏组织的超氧化物歧化酶1(SOD1)、超氧化物歧化酶2(SOD2)、过氧化氢酶(Catalase)蛋白表达水平。结果与正常组比较,模型组小鼠的体质量、心脏质量均明显下降(P<0.05,P<0.01);LDH水平明显上升(P<0.05),CK水平有升高趋势(P>0.05);心肌纤维排列紊乱、断裂,心肌细胞出现空泡变性;小鼠心脏组织中的SOD1、SOD2及Catalase蛋白表达均明显下调(P<0.05)。与模型组比较,蒿甲醚组小鼠的体质量、心脏质量均有所升高(P>0.05);LDH、CK水平均有降低(P>0.05);心肌细胞排列较均匀,核固缩和空泡变性明显减少;心脏组织中的SOD1、SOD2及Catalase蛋白表达均明显上调(P<0.05,P<0.01)。结论蒿甲醚对阿霉素诱导的小鼠心肌损伤具有一定保护作用,其作用机制可能与上调SOD1、SOD2、Catalase蛋白表达,调节氧化应激相关。

ObjectiveTo investigate the protective effect of artemether on adriamycin induced cardiac injury in mice.MethodsMale BALB/c mice were randomly divided into normal group, model group and artemether group(3 g·kg^(-1)),with 6 mice in each group. Mice model of cardiac injury induced by adriamycin was established. Body mass and heart mass of mice in each group were measured. Serum lactate dehydrogenase(LDH)and creatine kinase(CK) levels were detected. Hematoxylin-eosin(HE)staining was used to observe the cardiac histopathology of heart tissue in mice. The protein expression levels of superoxide dismutase 1(SOD1),superoxide dismutase 2(SOD2)and Catalase in heart tissues of mice in each group were detected by Western Blot and immunohistochemistry.Results Compared with normal group,body mass and heart mass of model group were significantly decreased(P<0.05,P<0.01);LDH level was significantly increased(P<0.05), CK level showed an increasing trend(P>0.05);Myocardial fibers were disordered and broken, and myocardial cells showed vacuolar degeneration;The protein expressions of SOD1, SOD2 and Catalase in mice heart tissue were significantly down-regulated(P<0.05).Compared with model group,the body weight and heart weight of artemether group were increased(P>0.05);LDH and CK levels were decreased(P>0.05). Cardiomyocytes are more evenly arranged, and the karyopyknosis and vacuolar degeneration were significantly reduced;The protein expression of SOD1, SOD2 and Catalase in heart tissue were significantly up-regulated(P<0.05,P<0.01).ConclusionArtemether has certain protective effect on adriamycin-induced cardiac injury in mice, and its mechanism of action may be related to the upregulation of protein expression on SOD1,SOD2 and Catalase and the regulation of oxidative stress.