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作 者:吴勇军[1] 喻嵘[1] 成细华[1] 吴慧[1] 夏金华[1]
出 处:《湖南中医药大学学报》2010年第9期43-46,共4页Journal of Hunan University of Chinese Medicine
基 金:国家自然科学基金项目(30973749);湖南省自然科学基金杰出青年基金项目(08JJ1005);湖南省中医药科研基金重点项目(2009003);湖南省高校创新平台开放基金项目(09K059);中西医结合临床重点学科资助
摘 要:目的观察左归复方治疗MKR小鼠后糖代谢及骨骼肌PPARγ和GLUT-4表达的变化。方法 40只MKR小鼠经鉴定后,随机分为MKR模型组、左归复方高、低剂量组、文迪雅组,每组10只。C57野生鼠10只作为空白对照组。各药物组分别以相应剂量连续给药30 d。于给药前、第15天及第30天,分别作空腹血糖测定。末次给药后0.5 h,心脏取血,放射免疫法测血清胰岛素,RT-PCR和免疫组化检测PPARγ和GLUT-4在骨骼肌中的表达。结果 (1)左归复方干预治疗后,其高剂量具有显著的降低MKR小鼠空腹血糖、改善高胰岛素血症的作用,差异有统计学意义(P<0.05,P<0.01);(2)MKR小鼠骨骼肌中PPARγ和GLUT-4 mRNA表达下调,与C57野生鼠比较差异具有统计学意义(P<0.01);左归复方干预治疗后,MKR小鼠骨骼肌中PPARγ和GLUT-4 mRNA表达均上调,左归复方上调PPARγ和GLUT-4 mRNA表达与阳性对照药文迪雅作用相当;(3)MKR小鼠骨骼肌中PPARγ蛋白表达下调,与C57野生鼠比较差异具有统计学意义(P<0.01);左归复方干预治疗后,PPARγ蛋白表达明显上调,差异有统计学意义(P<0.01),并与对照药文迪雅作用相当。结论左归复方具有显著的改善MKR小鼠糖代谢作用,其机制与上调骨骼肌中PPARγ和GLUT-4表达,增强骨骼肌对胰岛素的敏感性,促进骨骼肌摄取血液中葡萄糖有关。Objective To observe the ef fect of of Zuogui recipe(ZR) on glucose metabolism and PPARγ and GLUT-4 expression in the skeletal muscle of MKR mice.Methods Forty qualified MKR mice were equally randomized into 4 groups:model group(MG),low-dose ZP group(LZP),high-dose-ZP group(HZP) and positive control group(PCG).LZP,HZP and PCG were treated by corresponding drugs for 30 days.Using C57 mice as the controls,the fasting blood glucose(FBG) level and the serum insulin level were determined;the expression of PPARγmRNA and GLUT-4mRNA in the skeletal muscle were determined by RT-PCR,and the expression of PPARγ protein in the skeletal muscle was determined by SABC immunohistochemistry.Results Hyperglycemia in HZP was significantly ameliorated and fasting blood glucose was decreased after treatment(P0.05 or P0.01).Comparing with C57 mice,the expression of PPARγmRNA and GLUT-4mRNA in the skeletal muscle of model group were decreased(P 0.01).After treatment,the expression of PPARγmRNA and GLUT-4mRNA in the skeletal muscle of HZP and LZPgroups were significantly increased,compared with the model group.Conclusion Zuogui Recipe has obvious effect on improving glucose metabolism in MKR mice,and its mechanism may be related to the increase of PPARγand GLUT-4 expression in skeletal muscle,the increase of sensitivity of peripheral tissue to insulin,and the improvement of insulin resistance in the mice.
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