气虚血瘀大鼠模型糖、脂代谢及氧化应激反应研究  

Glucose and lipid metabolism and oxidative stress reaction in rat model of qi-deficiency and blood-stasis syndrome

作　　者：扈新刚[1] 张允岭[2] 郑宏[2] 张锦[2] 闫妍[2] 黄启福[3] 

机构地区：[1]北京中医药大学第三附属医院,北京100029 [2]北京中医药大学东方医院 [3]北京中医药大学基础医学院

出　　处：《北京中医药大学学报》2009年第4期249-251,共3页Journal of Beijing University of Traditional Chinese Medicine

基　　金：国家重点基础研究发展计划(973计划)资助项目(No.2003CB517104)

摘　　要：目的从糖、脂代谢及心、脑组织氧化应激损伤等角度,探讨气虚血瘀大鼠模型靶器官损伤及其机理。方法采用力竭游泳法制作气虚血瘀大鼠模型,分别造模1、2、4周,然后检测模型大鼠血糖、血脂及心、脑组织丙二醛(MDA)、超氧化物歧化酶(SOD)水平。结果模型组大鼠力竭造模后1、2、4周血糖均升高,血浆总胆固醇(TC)及甘油三酯(TG)水平在4周时下降,高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)未见明显异常变化;模型组大鼠心肌组织MDA含量升高,心肌组织SOD及脑组织MDA、SOD未见有显著性意义的变化。结论糖、脂等能量代谢紊乱是气虚血瘀证重要生物学基础,其靶器官的损害可能与氧化应激损伤密切相关。Objective To investigate the target organ lesion and its mechanism in rat model of qideficiency and blood-stasis syndrome from the aspect of glucose and lipid metabolism and oxidative stress reaction of heart and brain tissue. Method The rat model of qi-deficieney and blood-stasis syndrome was established by using exhaustive swimming. After 1,2 or 4 weeks the levels of blood glucose, blood lipid, serum lipoprotein, and the contents of malondialdehyde （MDA） and superoxide dismutase （SOD） of heart and brain tissue were detected respectively. Result In the model group the level of blood glucose increased after 1, 2 or 4 weeks. The levels of plasma total cholesterol （TC） and triglyeeride （TG） decreased, and high-density lipoprotein-C （HDL-C） and low-density lipoprotein-C （LDL-C） had no changes after 4 weeks. The content of heart MDA increased, and the contents of heart SOD, brain MDA and SOD had no significant changes in rats of model group. Conclusion The disorder of glucose and lipid metabolism is an important biological basis of qi-defieiency and blood-stasis syndrome. The target organ lesion may be related closely to oxidative stress reaction.

关 键 词：力竭游泳 气虚血瘀 能量代谢 氧化应激 大鼠 

分 类 号：R285.5[医药卫生—中药学]