摘要
目的:探讨还少丹对D-半乳糖(D-galactose,D-gal)诱导的衰老模型小鼠心肌线粒体结构与功能的影响。方法:将小鼠随机分为空白对照组、衰老模型组、还少丹低、高剂量组。采用D-gal建立衰老模型,还少丹水煎液灌胃6周。以差速离心法分离小鼠心肌组织线粒体;Comas亮蓝蛋白定量法测定线粒体蛋白含量;分光光度法检测线粒体呼吸链复合体I和复合体Ⅳ的活性,以及Na+-K+-ATP酶和Ca2+-ATP酶的活性。结果:衰老模型组复合体I和复合体Ⅳ的活性明显降低(分别为P<0.05和P<0.01),还少丹低、高剂量组均能明显提高复合体I和复合体Ⅳ的活性(P<0.01)。衰老模型组Na+-K+-ATP酶和Ca2+-ATP酶活性明显降低(分别为P<0.05和P<0.01),还少丹各剂量组均能明显提高Na+-K+-ATP酶活性(P<0.01),还少丹低、高剂量组间Ca2+-ATP酶活性的差异无统计学意义(P>0.05)。结论:还少丹具有保护小鼠心肌线粒体结构、增强心肌线粒体功能的作用。
Objective To investigate the effect of huanshaodan on myocardial mitochondrial structure and function in aged mice induced by D-galactose（D-gal）.Methods Mice were divided randomly into a blank control group,an aged model group,a low dose huanshaodan group,and a high dose huanshaodan group.The aged model was established by injecting D-gal.After feeding with huanshaodan for 6 weeks,mitochondria were obtained from heart of mice by differential centrifugation.Protein content of mitochondria was determined by coomassie blue staining.Then spectrophotometry was used to detect the activities of mitochondrial respiratory chain Complex Ⅰ and Ⅳ,Na^＋-K^＋-ATPase,and Ca^2＋-ATPase.Results The activities of Complex Ⅰ and Ⅳ in the aged model group were significantly reduced（P〈0.05 and P〈0.01）,whereas the activities of Complex Ⅰ and Ⅳ were both elevated significantly in the low and high dose huanshaodan groups（P〈0.01）.The activities of Na^＋-K^＋-ATPase and Ca^2＋-ATPase in the aged model group were obviously depressed（P〈0.05 and P〈0.01）,and the activities of Na^＋-K^＋-ATPase in the low and high dose huanshaodan groups were visibly increased（P〈0.01）,but the activities of Ca^2＋-ATPase showed no changes in the low and high dose huanshaodan groups（P〉0.05）.Conclusion Huanshaodan,decoction of Chinese herbal medicine can protect the structure of myocardial mitochondria and enhance the function of myocardial mitochondria in mice.
出处
《国际病理科学与临床杂志》
CAS
2011年第2期93-97,共5页
Journal of International Pathology and Clinical Medicine
基金
湖南省教育厅科研课题(07C479)~~
关键词
中草药水煎液
衰老
心肌
线粒体功能
小鼠
decoction of Chinese herbal medicine
aging
myocardia
mitochondrial function
mice
