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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
Objective :To investigate the protective effect of glycosides of cistanche (GCs) on myocardial injury induced by doxorubicin (Dox) in mice and its mechanism. METHODS: The model of acute myocardial injury induced by intraperitoneal injection of Dox (17.5 mg/kg) in NIH mice was used to determine the activity of superoxide dismutase (SOD) in the heart muscle; selenium-glutathione peroxidase (Se- GSH-Px) Activity; malondialdehyde (MDA) content and serum creatine kinase (CPK) activity. Electron microscopy examined the ultrastructural changes in myocardial cells. RESULTS: Intraperitoneal injection of Dox for 48 hours could induce myocardial damage, SOD activity and Se-GSH-Px activity in myocardium, MDA content increased, activity of CPK in serum increased, and myocardial ultrastructural damage appeared. GCs (62.5,125.0,25.0 mg/kg) increased myocardial SOD, Se-GSH-Px activity, decreased MDA content, decreased CPK release, and reduced myocardial ultrastructural damage. CONCLUSION: Glycosides of Cistanche have a protective effect on myocardial damage induced by doxorubicin. Its mechanism may be related to the protection of myocardial SOD and Se-GSH-Px activity and the scavenging of free radicals and the prevention of lipid peroxidation.