【摘要】 目的 :探讨肉苁蓉总苷 (GCs)对阿霉素 (Dox)所致小鼠心肌损害的保护作用及其机制。 方法 :选用NIH小鼠一次腹腔注射 Dox(17.5 m g/ kg)造成急性心肌损伤模型 ,测定心肌超氧化物歧化酶 (SOD)活性 ;硒 -谷胱苷肽过氧化物酶 (Se- GSH - Px)活性 ;丙二醛 (MDA)含量及血清肌酸磷酸激酶 (CPK)活性。电镜检查心肌细胞超微结构的改变。结果 :腹腔注射 Dox 4 8h后可致小鼠心肌明显损害 ,心肌 SOD及 Se- GSH- Px活性下降 ,MDA含量升高 ,血清中 CPK的活性增强 ,同时出现心肌组织超微结构的损伤。 GCs(6 2 .5、12 5 .0、2 5 0 .0 m g/ kg)能增加心肌SOD、Se- GSH- Px活性 ,降低 MDA含量 ,减少 CPK释放 ,减轻心肌超微结构的损伤。 结论:肉苁蓉总苷对阿霉素所致心肌损害有一定的保护作用 ,其机制可能与其保护心肌 SOD及 Se- GSH- Px活性及其清除自由基 ,防止脂质过氧化有关更多还原

【Abstract】 Objective: To investigate the protective effect of glycosides of cistanche(GCs) against doxorubicin induced cardiotoxicity in mice and its mechanism. Methods: NIH mice were treated intraperitoneally with doxorubicin (Dox) at a single dose of 17.5 mg/kg -1 to develop an acute myocardium injury model. The activity of SOD, GSH Px ,the content of MDA and the activity of creatine phosphokinase(CPK) was measured. The cardiac ultrastructureal changes were examined with scanning electron microscope. Results: At the 48h after administration, Dox elicited severe myocardial damage with decreasing myocardial SOD and GSH Px activity, increasing myocadial MDA content and serum CPK activity in mice. It also caused severe myocardial cell damage at ultrastructure level. Oral administration of GCs (62.5,125,250 mg/kg -1 ) protected against these changes induced by Dox, by increasing myocardial SOD, GSH Px activity, decreasing myocadial MDA content and serum CPK activity and reducing cardiotoxicity of Dox at the ultrastructural level. Conclusion: The glycosides of cistanche has protective effect on cardiotoxicity induced by Dox. The mechanisms of reduced cardiotoxicity induced by Dox may depend on the effect of GCs on scavenging oxygen free radials in mice heart, protecting the activity of SOD and GSH Px and inhibiting lipid peroxidation.更多还原