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灵芝多糖对2型糖尿病大鼠胸主动脉AGEs 及其受体的影响
引用本文:陈杨,乔进,罗佳,吴锋,孟国梁,陈惠,郑惠华,徐济良. 灵芝多糖对2型糖尿病大鼠胸主动脉AGEs 及其受体的影响[J]. 中国中药杂志, 2011, 36(5): 624-627
作者姓名:陈杨  乔进  罗佳  吴锋  孟国梁  陈惠  郑惠华  徐济良
作者单位:1. 南通大学医学院,药理教研室,江苏,南通,226001
2. 江苏安惠生物科技有限公司,江苏,南通,226006
基金项目:国家科技部"十一五"科技支撑计划(2006DAI06A20- 02);南通大学校级自然科学研究项目(09Z036);南通大学研究生科技创新计划项目(YKC09038)
摘    要:
目的:研究灵芝多糖对2型糖尿病大鼠胸主动脉糖基化终末产物及其受体的影响,探讨灵芝多糖对糖尿病大鼠主动脉的保护机制.方法:SD大鼠经4周高脂饮食后腹腔注射链脲佐菌素(STL)30mg·㎏-1建立2型糖尿病(T2DM)模型.大鼠随机分为对照组、模型组、小檗碱阳性对照组、灵芝多糖低、中、高剂量组(200,400,800mg·㎏-1).给药治疗12周后,测定大鼠空腹血糖、血清中糖基化终末产物(AGES)含量,免疫组化法和蛋白印迹法测定胸主动脉AGES,RAGE蛋白的表达情况.结果:灵芝多糖高、中剂量组与模型组大鼠相比,血糖和血清AGES明显降低(P<0.01).各治疗组胸主动脉AGE.和RAGE的表达量较模型组都有所下调,其中灵芝多糖高剂量组表达明显下调(P<0.01).结论:灵芝多糖对T2DM大鼠血糖的降低和主动脉保护作用明显,其机制可能是下调AGES及RAGE的表达从而对糖尿病大鼠主动脉起到保护作用.

关 键 词:灵芝多糖  糖尿病  糖基化终末产物  糖基化终末产物特异性受体
收稿时间:2010-07-12

Effects of Ganoderma lucidum polysaccharides on advanced glycation end products and receptor of aorta pectoralis in T2DM rats
CHEN Yang,QIAO Jin,LUO Ji,WU Feng,MENG Guoliang,CHEN Hui,ZHENG Huihua and XU Jiliang. Effects of Ganoderma lucidum polysaccharides on advanced glycation end products and receptor of aorta pectoralis in T2DM rats[J]. China Journal of Chinese Materia Medica, 2011, 36(5): 624-627
Authors:CHEN Yang  QIAO Jin  LUO Ji  WU Feng  MENG Guoliang  CHEN Hui  ZHENG Huihua  XU Jiliang
Affiliation:Department of Pharmacology, Medical College, Nantong University, Nantong 226001, China;Department of Pharmacology, Medical College, Nantong University, Nantong 226001, China;Department of Pharmacology, Medical College, Nantong University, Nantong 226001, China;Department of Pharmacology, Medical College, Nantong University, Nantong 226001, China;Department of Pharmacology, Medical College, Nantong University, Nantong 226001, China;Jiangsu Anhui Biological Technology Co., Ltd., Nantong 226006, China;Jiangsu Anhui Biological Technology Co., Ltd., Nantong 226006, China;Department of Pharmacology, Medical College, Nantong University, Nantong 226001, China
Abstract:
Objective : To investigate the effects of Ganoderma lucidum polysaccharides(GLPs)on advanced glycation end products(AGEs) and the receptor (RAGE)of aorta pectoralis in the T2DM rats, and explore the protective mechanism of GLPs on the aorta pectoralis. Method : SD rats were fed with high-fat diet for 4 weeks and then were injected STZ (30 mg·kg-1) to induce the type 2 diabetic rats. Once the T2DM models were set successfully, rats were randomly divided into normal control group, diabetes model (DM) group, berberine (30 mg·kg-1) group, GLPs of low (GLPs-L), middle(GLPs-M) and high-dose(GLPs-H) group (GLPs were orally given 200, 400, 800 mg·kg-1). After 12 weeks' treatment, the content of fasting blood glucose and AGEs in serum were detected. The expressions of AGEs and RAGE in aortas pectoralis were measured both by immunohistochemistric assays and western-blot analysis. Result : Compared with DM group, the content of blood glucose and AGEs in serum were significantly decreased in GLPs-H group and GLPs-M group (P<0.01). Compared with DM group, the expressions of AGEs and RAGE in aorta pectoralis were decreased in other groups, especially in GLPs-H group(P<0.01). Conclusion : GLPs could low blood glucose and protect aortas effectively. The mechanisms may be involved in down-regulation the expressions of AGEs and RAGE in aortal tissue.
Keywords:Ganoderma lucidum polysaccharides  diabetes mellitus  advanced glycation end products  advanced glycosylation end product-specific receptor
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