表没食子儿茶素没食子酸酯干预柔红霉素致小鼠心肌损伤的疗效观察

目的 观察1,6-二磷酸果糖(FDP)与表没食子儿茶素没食子酸酯(EGCG)对柔红霉素介导的小鼠心肌毒性的预防作用。 方法 将昆明种小鼠采用随机数字表法随机分为正常对照组、模型组、FDP组、EGCG组,每组20只,其中FDP、EGCG两组分别灌胃给予FDP与EGCG 40 mg/kg,对照组和模型组同时灌胃给予等体积生理盐水(NS)。给药一周后,除正常对照组腹腔注射等体积的生理盐水(NS)外,其余各组均腹腔注射给予柔红霉20 mg/kg,给予柔红霉素48 h后测定各组小鼠血清心肌酶[肌酸激酶同工酶(CK-MB)、谷草转氨酶(AST)、-羟基丁酸脱氢酶(-HBDH)]水平,采用SPSS 19.0统计软件对数据进行统计分析。 结果 对照组小鼠存活率为100%,而模型组与对照组比较,存活率明显下降(60%),且其血清心肌酶指数升高(P<0.01);FDP组、EGCG组分别与模型组比较,存活率升高(90%),而心肌酶指数均有所降低(P<0.01),其中EGCG组心肌酶指数下降更为明显(P<0.05)。 结论 FDP及EGCG可减轻柔红霉素对小鼠的心肌毒性,而EGCG疗效相对FDP可能更佳。 

Effect of epigallocatechin gallate on daunorubicin-induced cardiotoxicity in mice

Objective To observe the prevention effect of Fructose-1, 6-diphosphate (FDP) and Epigallocatechin gallate (EGCG) against the daunorubicin-induced myocardial injury in mice. Methods The Kunming mice were randomly divided into normal control group, model group, positive control group (FDP group), drug intervention group (EGCG group), with 20 mice in each group. The mice in the FDP group and EGCG group were given FDP and EGCG (40 mg/kg) by intragastric administration, and the mice in the normal control group and model group were given equal volume of normal saline. One week later, the mice in the model group, FDP group and EGCG group were given daunorubicin (20 mg/kg) by intraperitoneal injection, while in the control group were given normal saline. Forty-eight hours after daunorubicin was administrated, All the mice were taken the blood to test the levels of myocardial enzyme (CK-MB, AST, -HBDH). The experimental data were analyzed by using SPSS 19.0. Results The survival rate of normal control group was 100%, which was higher than that of the model group (60%); however, the level of myocardial enzyme in the model group was higher than that in the control group (P<0.01). The survival rate (90%) of both FDP group and EGCG group was higher than that of the model group, and the level of myocardial enzyme was decreased (P<0.01), especially in the EGCG group (P<0.05). Conclusion FDP and EGCG can depress the cardiotoxicity of daunorubicin in mice, especially the latter.