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作 者:金鑫[1] 张会欣[1,2] 张彦芬 秘尧 何其龙 崔雯雯[1] 周升山
机构地区:[1]黑龙江中医药大学,哈尔滨150040 [2]河北以岭医药研究院,石家庄050035 [3]国家中医药管理局重点研究室心脑血管络病,石家庄050035 [4]河北省络病重点实验室,石家庄050035
出 处:《中国实验动物学报》2015年第1期69-74,共6页Acta Laboratorium Animalis Scientia Sinica
基 金:国家重点基础研究发展计划(973计划)项目(编号:2012CB518606)
摘 要:目的探究津力达对高脂诱导的胰岛素抵抗Apo E-/-小鼠骨骼肌甘油三酯相关基因的影响。方法将8只雄性C57BL/6J小鼠设为正常组(A组);40只雄性Apo E-/-小鼠喂养16周后分为模型组(B组)、罗格列酮组(C组)、津力达低剂量组(D组)、津力达中剂量组(E组)、津力达高剂量组(F组),开始灌胃给药,连续8周。采用酶法、BCA蛋白浓度法测定骨骼肌TG含量;OGTT评价小鼠的胰岛素抵抗程度;RT-PCR和Western blot测定小鼠骨骼肌HSL、ATGL、PPARγmRNA和蛋白表达。结果津力达能够不同程度降低小鼠的FBG、TC、TG和LDLC,升高HDL-C;下调FIns水平,提高ISI,明显改善小鼠糖耐量异常;津力达能够不同程度的上调小鼠HSL、ATGL、PPARγmRNA和蛋白表达。结论津力达能够通过调节骨骼肌甘油三酯相关酶的表达,改善高脂诱导的Apo E-/-小鼠的胰岛素抵抗。Objective To investigate the effect of the Chinese medicine Jinlida on triglyceride-related genes in skeletal muscle of fat-induced insulin resistant ApoE^-/- mice. Methods Eight male C57BL/6J mice were set to the nor- mal group (group A). Forty male ApoE^-/ - mice were fed high-fat diet for 16 weeks and divided into model group (group B) , rosiglitazone ( group C) , Jinlida low dose group ( group D) , Jinlida moderate dose group ( group E) , Jinlida high- dose group ( group F) , and giving gavage for 8 weeks. TG content in the skeletal muscle was determined by enzymatic and BCA protein concentration assay. Oral glucose tolerance test (OGTT) was used to evaluate the degree of insulin resistance in the mice. Real-time fluorescent quantitative reverse transcription PCR (RT-PCR) and Western blot method were used to determine the expressions of hormone-sensitive lipase (HSL) , adipose triglyceride lipasc (ATGL) , and peroxisome prolif- erator-activated receptor gamma (PPAR'y) mRNA and proteins in the skeletal muscle. Results Jinlida to varying degrees lowered the fasting blood glucose (FBG) , cholesterol (TC) , triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) , increased the high density lipoprotein (HDL-C) , reduced fasting insulin (Fins) level and raised insulin sensi- tire index (IS1) , and significantly improved the abnormal glucose tolerance in the mice. Jinlida to a certain degree raised the levels of HSL, ATGL, PPAR3, mRNA and protein expressions. Conclusions Jinlida can alleviate fat-induced insulin resistance in ApoE^-/- mice through regulation of triglyceride-related gene expression.
关 键 词:津力达 APOE^-/-小鼠 胰岛素抵抗 骨骼肌甘油三酯相关基因
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