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作 者:金鑫[1] 张会欣[1,2] 崔雯雯[1,3,4]
机构地区:[1]黑龙江中医药大学,黑龙江哈尔滨150040 [2]河北以岭医药研究院,河北石家庄050000 [3]国家中医药管理局重点研究室(心脑血管络病),河北石家庄050000 [4]河北省络病重点实验室,河北石家庄050000
出 处:《中药材》2015年第6期1237-1241,共5页Journal of Chinese Medicinal Materials
基 金:国家重点基础研究发展计划(973计划)项目(2012CB518606)
摘 要:目的:研究津力达颗粒对高脂诱导的胰岛素抵抗Apo E-/-小鼠骨骼肌甘油三酯相关基因的影响。方法:8只雄性C57BL/6J小鼠设为正常对照组(NF);40只雄性Apo E-/-小鼠高脂饮食喂养16 w后分为模型组、罗格列酮组及津力达颗粒低、中、高剂量组,开始灌胃给药,连续8 w。采用酶法、BCA蛋白浓度法测定骨骼肌TG含量;葡萄糖耐量实验(OGTT)评价小鼠胰岛素抵抗程度;实时荧光定量反转录PCR(RT-PCR)和蛋白质印迹法(Western blot)测定小鼠骨骼肌胰岛素受体底物(IRS-1)、二酰甘油酰基转移酶1(DGAT1)mRNA和蛋白表达。结果:津力达颗粒能够不同程度降低小鼠的空腹血糖(FBG)、胆固醇(TC)、甘油三酯(TG)和游离脂肪酸(FFA);下调空腹胰岛素(FIns)水平,提高胰岛素敏感指数(ISI),显著改善小鼠糖耐量异常;明显改善小鼠骨骼肌脂质沉积;不同程度上调小鼠IRS-1 mRNA和蛋白表达,下调DGAT1 mRNA和蛋白表达。结论:津力达颗粒能通过调节骨骼肌DGAT1基因和蛋白表达,改善高脂诱导的Apo E-/-小鼠的胰岛素抵抗。Objective:To investigate the effect of Jinlida on DGAT1 in skeletal muscle in fat-induced insulin resistance ApoE -/- mice. Methods:Eight male C57BL/6J mice were used as normal group. 40 male ApoE-/- mice were fed high-fat diet for 16 weeks and divided into five groups:control group,rosiglitazone group, and Jinlida low, middle and high dose groups. Then corresponding drugs were administrated intragastrically for eight weeks. TG content in skeletal muscle was measured by enzymic enzymatic, Glucose tolerance test (OGTr) was used to evaluate the degree of insulin resistance in mice. The mRNA and protein expression of insulin receptor substrate (IRS-1) and diacylglycerol acyltransferase 1 (DGAT1)in skeletal muscle were measured by real-time quantitative reverse transcription PCR (RT-PCR) and Western blot. Results : Jinlida particles reduced fasting blood glucose ( FBG), cholesterol ( TC ), triglyceride ( TG ), free fatty acid(FFA) and fasting insulin(Fins) levels, raised insulin sensitive index (ISI), improved glucose tolerance, and reduced skel- etal muscle lipid deposition in ApoE -/- mice significantly. Jinlida particles increased the expression of IRS-1 mRNA and protein, and reduced DGAT1. Conclusion: Jinlida can alleviate the expression of DGAT1 in skeletal muscle in fat-induced insulin resistance ApoE-/- mice.
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