津力达对高脂诱导的胰岛素抵抗ApoE^(-/-)小鼠骨骼肌脂质转运酶类的表达变化  

Effect of Jinlida on changes in expression of skeletal muscle lipid transport enzymes in fat-induced insulin resistance ApoE^(-/-) mice

作　　者：金鑫[1] 张会欣[1,2] 张彦芬 崔雯雯[1] 秘尧 何其龙 周升山 

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国家中医药管理局重点研究室(心脑血管络病),河北石家庄050035 [3]河北省络病重点实验室,河北石家庄050035

出　　处：《中国中药杂志》2015年第6期1156-1160,共5页China Journal of Chinese Materia Medica

基　　金：国家重点基础研究发展计划(973)项目(2012CB518606)

摘　　要：目的:探究津力达对高脂诱导的胰岛素抵抗Apo E-/-小鼠骨骼肌脂质转运酶类相关基因的表达变化。方法:8只雄性C57BL/6J小鼠设为正常组(NF);40只雄性Apo E-/-小鼠喂养16周后分为模型组(HF)、罗格列酮组(LGLT)、津力达低剂量组(JLDL)、津力达中剂量组(JLDM)、津力达高剂量组(JLDH),开始灌胃给药,连续8周。采用组织游离脂肪酸、BCA蛋白浓度法测定骨骼肌FFA含量;实时荧光定量反转录PCR(RT-PCR)和蛋白质印迹法(Western blot)测定小鼠骨骼肌脂肪酸转位酶(FAT/CD36)、肉毒碱棕榈酰基转移酶1(CPT1)、过氧化物酶体增殖物激活受体α(PPARα)mRNA和蛋白表达。结果:津力达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);津力达能够不同程度的上调小鼠CPT1,PPARαmRNA和蛋白表达,下调FAT/CD36的mRNA和蛋白水平。结论:津力达能够通过调节骨骼肌脂质转运酶类的表达变化,改善高脂诱导的Apo E-/-小鼠的胰岛素抵抗。Objective： To study the effect of Jinlida on changes in expression of skeletal muscle lipid transport enzymes in fat-induced insulin resistance Apo E-/-mice. Method： Eight male C57 BL /6J mice were selected in the normal group（ NF）,40 male Apo E-/-mice were fed for 16 weeks,divided into the model group（ HF）,the rosiglitazone group（ LGLT）,the Jinlida low-dose group（ JLDL）,the Jinlida medium-dose group（ JLDM）,the Jinlida high-dose group（ JLDH） and then orally given drugs for 8weeks. The organization free fatty acids,BCA protein concentration determination methods were used to determine the skeletal muscle FFA content. The Real-time fluorescent quantitative reverse transcription PCR（ RT-PCR） and Western blot method were adopted to determine mRNA and protein expressions of mice fatty acids transposition enzyme（ FAT / CD36）,carnitine palm acyltransferase 1（ CPT1）,peroxide proliferators-activated receptor α（ PPAR α）. Result： Jinlida could decrease fasting blood glucose（ FBG）,cholesterol（ TC）,triglyceride（ TG）,free fatty acid（ FFA） and fasting insulin（ FIns） and raise insulin sensitive index（ ISI） in mice to varying degrees. It could also up-regulate mRNA and protein expressions of CPT1 and PPARα,and down-regulate mRNA and protein levels of FAT / CD36. Conclusion： Jinlida can improve fat-induced insulin resistance Apo E-/-in mice by adjusting the changes in expression of skeletal muscle lipid transport enzymes.

关 键 词：津力达 APOE-/-小鼠 胰岛素抵抗 骨骼肌脂质转运酶 

分 类 号：R285.5[医药卫生—中药学]