摘要
目的:研究luteolin对链脲佐菌素诱导的I型糖尿病大鼠心功能及心肌线粒体氧化应激的影响。方法:雄性SD大鼠,随机分成正常对照组,luteolin对照组,糖尿病模型组,低剂量luteolin(10 mg/(kg.d))灌胃治疗组,高剂量luteolin(100 mg/(kg.d))灌胃治疗组。各组大鼠饲养8周后,测体重、血糖、心功能、左心室重量、心肌胶原含量及活性氧自由基(ROS)水平,分离心肌线粒体检测ROS水平、超氧化物歧化酶(SOD)活性及线粒体肿胀程度。结果:luteolin处理对糖尿病大鼠血糖无明显影响,但可减少糖尿病引起的体重下降。高剂量luteolin可显著减小糖尿病大鼠心室与体重比值,提高左室发展压,降低左室舒张末压。高剂量luteolin治疗后,糖尿病大鼠心肌ROS及胶原含量,心肌线粒体ROS水平与肿胀程度均明显下降,心肌线粒体SOD活性明显增加。结论:luteolin处理可显著改善糖尿病大鼠心功能,其机制可能与减轻心肌线粒体氧化应激及抑制线粒体肿胀有关。
Objective: To investigate the effects of luteolin (Chinese Traditional Medicine) on cardiac functions and mitechondrial oxidative stress in streptozotocin (STZ)-induced diabetic rats. Methods: Male SD rats were randomly divided into a normal control group, a luteolin control group, a diabetic group, and diabetic groups orally administered with a low dose (10 mg/(kg·d) ) or a high dose of lutcolin (100 mg/ (kg·d)) for eight weeks. The body weight, blood glucose, cardiac functions, left ventricular weight, myocardial collagen and reactive oxygen species (ROS) levels were assayed. The cardiac mitochondrial ROS level, superoxide dismutase (SOD) activity and the mitochondrial swelling were measured. Results: Treatment with luteolin had no effect on the blood glucose but reduced the losing of body weight in diabetic rats. High dose of luteolin markedly reduced the ratio of ventricular weight and body weight, increased the left ventricular develop pressure, and decreased the left ventricular end diastolic pressure in diabetic rats. The myocardial levels of ROS and collagen, the cardiac mitochondrial ROS level, and the mitochondrial swelling in diabetic rats were all markedly reduced by high dose of luteolin. Furthermore, high dose of luteolin significantly increased the mitochondrial SOD activity in diabetic rat hearts. Condusion: Treatment with luteolin for 8 weeks markedly improves the cardiac function, which may be related to reducing mitochondrial oxidative stress and mitochondrial swelling in diabetic rats.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2011年第4期409-414,共6页
Chinese Journal of Applied Physiology
基金
浙江省自然科学基金资助项目(Y206179)