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目的研究表没食子儿茶素没食子酸酯(EGCG)全乙酰化衍生物(AcEGCG)对柔红霉素(DNR)致小鼠心脏毒性的影响。方法 80只小鼠随机分为4组(n=20):正常组、DNR致心脏毒性模型组、AcEGCG高剂量组(80 mg·kg-1)、AcEGCG低剂量组(40 mg·kg-1)。采用腹腔注射DNR(15mg·kg-1)制备小鼠心脏毒性模型。检测小鼠心电图、血清心肌酶谱、高敏肌钙蛋白T(TNT-Hs)、超氧化物歧化酶(SOD)、丙二醛(MDA),电镜观察心肌超微结构。结果DNR可导致小鼠心律失常,血淸心肌酶谱和TNT-Hs明显升高,血清和心肌SOD活性降低,MDA含量增多,心肌超微结构损伤;而AcEGCG可拮抗DNR所致上述变化。结论AcEGCG对DNR致小鼠心脏毒性具有保护作用,其作用机制可能与增强SOD活力和抗脂质过氧化有关。
Objective To study the effect of epicatechin gallate (EGCG) acetylated derivatives (AcEGCG) on cardiotoxicity induced by daunorubicin (DNR) in mice. Methods Eighty mice were randomly divided into 4 groups (n = 20): normal group, DNR induced cardiotoxicity model group, AcEGCG high dose group (80 mg · kg -1), AcEGCG low dose group (40 mg · kg -1 ). The mouse cardiotoxicity model was prepared by intraperitoneal injection of DNR (15 mg · kg-1). The electrocardiogram, serum myocardial enzymes, high-sensitivity troponin T (TNT-Hs), superoxide dismutase (SOD), malondialdehyde (MDA) Results DNR induced cardiac arrhythmia, myocardial enzymes in serum and TNT-Hs significantly increased, serum and myocardial SOD activity decreased, MDA content increased myocardial ultrastructure damage; and AcEGCG can antagonize the above changes caused by DNR. Conclusion AcEGCG has a protective effect on cardiotoxicity induced by DNR in mice, and its mechanism may be related to the enhancement of SOD activity and anti-lipid peroxidation.