摘要
目的探讨右丙亚胺对表柔比星致大鼠心肌损伤的保护作用及其机制,为临床用药提供实验依据。方法将35只SD大鼠随机分为5组:正常对照组、模型组(表柔比星+生理盐水)、表柔比星+低剂量右丙亚胺组(DEX1)、表柔比星+中剂量右丙亚胺组(DEX2)、表柔比星+高剂量右丙亚胺组(DEX3),给药后检测各组大鼠心肌组织微量丙二醛(MDA)含量、总超氧化物歧化酶(T-SOD)活性和血浆乳酸脱氢酶(LDH)水平并观察心肌细胞凋亡的情况。结果与正常对照组比较,模型组大鼠心肌组织的SOD活性明显降低,MDA含量、血浆LDH含量和心肌细胞凋亡指数均明显升高(P<0.01);而与模型组比较,用右丙亚胺处理的各组大鼠心肌组织SOD活性明显升高,心肌组织MDA含量、心肌细胞凋亡指数及血浆LDH含量均显著降低(P<0.01或P<0.05)。结论右丙亚胺能减少表柔比星所致的心肌细胞凋亡,可能与其降低氧自由基的产生和脂质过氧化产物含量有关。
Objective To explore the effects of dexrazoxane on pharmorubicin induced myocardial damage and its mechanisms. Methods 35 SD rats were randomly divided into five groups： control group, model group（epirubicin＋saline）; DEX1 group（epirubicin＋low dose of dexrazoxane）; DEX2 group（epirubicin＋medium dose of dexrazoxane）; DEX3 group（epirubicin＋high dose of dexrazoxane）. After administration, we detected the malondialdehyde（MDA） content and total superoxide dismutase（T-SOD） activity in myocardial tissues, plasma lactate dehydrogenase（LDH） levels of each group, and observed cardiomyocyte apoptosis in all groups. Results Compared with the control group, the SOD activity in myocardial tissue of model group was significantly decreased, and the MDA content in myocardial tissue, the plasma LDH content, and myocardial cell apoptotic index were significantly increased（P〈0.01）. Compared with the model group, the SOD activity in myocardial tissue of rats treated by different doses of dexrazoxane was markedly increased, and the MDA content in myocardial tissue, the plasma LDH content, and myocardial cell apoptotic index were significantly decreased（P〈0.01 or P0.05）. Conclusion Dexrazoxane could relieve pharmorubicin-induced myocardial apoptosis. This may be associated with that it could reduce the produce of oxygen radical and lipid peroxidation.
出处
《肿瘤药学》
CAS
2014年第1期40-45,共6页
Anti-Tumor Pharmacy
基金
湖南省卫生厅资助项目(B2012-094)
