表没食子儿茶素没食子酸酯全乙酰化衍生物对柔红霉素致小鼠心脏毒性的影响

Effects of (-)-epigallocatechin-3-gallate peracetylated derivative on daunorubicin-induced cardiotoxicity in mice

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。

Aim To study the effects of(-)-epigallocatechin-3-gallate peracetylated derivative(AcEGCG)on daunorubicin(DNR)-induced cardiotoxicity in mice. Methods Eighty mice were randomly divided into four groups(n = 20) : normal control group,DNR-induced myocardial injury model group, high dosage of AcEGCG group(80 mg · kg- 1) and low dosage of AcEGCG group(40 mg ·kg- 1). DNR(15mg · kg- 1) was injected intraperitoneally to induce myocardial injury model in mice. The electrocardiogram,the activities of myocardial enzymes and the levels of cardiac troponin T hs(TNT-Hs) in serum,the activities of SOD and the contents of MDA in serum and myocardium were measured. With transmission electron microscope,the cardiac ultrastructural changes were observed. Results DNR increased the incidence of arrhythmia,increased the activities of myocardial enzymes and the levels of TNT-Hs in serum,decreased the activities of SOD,increased the contents of MDA in serum and myocardium,injured myocardial ultrastructure in mice. Compared with model group,AcEGCG could prevent the alteration of the abovementioned indexes. Conclusions AcEGCG has protective effects on DNR-induced cardiotoxicity in mice.The mechanism may be related to its enhancing SOD activities and anti-lipid peroxidation.