Effect of Huangqi Gegen Decoction on Insulin Resistance and Gene Expression of PPAR-γ in Type 2 Diabetes Mellitus Rats
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摘要:
目的: 观察黄芪葛根汤对2型糖尿病大鼠胰岛素抵抗及脂肪组织中过氧化物酶体增生物激活受体-γ(PPAR-γ)mRNA表达的影响。 方法: 雄性SD大鼠高脂饲料喂养4周后注射小剂量链脲佐菌素,1周后测定大鼠空腹血糖(FBG)及糖负荷2 h后血糖(2 h BG),选择FBG正常及2 h BG≥7.8 mmol·L-1者为模型大鼠。取模型大鼠,随机分为模型对照组、罗格列酮组,黄芪葛根汤高、中、低剂量组,另设正常对照组,药物干预8周后,测定FBG,空腹胰岛素水平(FINS),血浆瘦素(Leptin),肿瘤坏死因子-α(TNF-α),计算胰岛素敏感指数(ISI)和抵抗指数(HOMA-IR),提取大网膜脂肪组织总RNA,采用逆转录PCR技术扩增PPAR-γ基因片段,检测其基因表达水平。 结果: 黄芪葛根汤能提高模型大鼠ISI,降低HOMA-IR指数,降低Leptin和TNF-α水平,增加PPAR-γ mRNA表达。 结论: 黄芪葛根汤对大鼠IR具有显著的改善作用,其机制可能与降低血浆Leptin,TNF-α水平,提高脂肪组织PPAR-γ mRNA表达有关。
Abstract:
Objective: To observ effect of Huangqi Gegen decoction on insulin resistance(IR) and gene expression of peroxisome proliferator-activated receptor-γ(PPAR-γ) in type 2 diabetes mellitus(T2DM) rats. Method: Male Wistar rats were randomly divided into nomal group,model proup.The rats of normal group were fed with common food while the others with high calorie food for 4 weeks and injected with low dose of STZ. The level of fasting blood glucose(FBG) and 2 hours blood glucose(2 h BG) of glucose load were measured by routin method in rats with hyperlipemia after one week. The rats with nomal FBG level and 2 hBG level ≥7.8 mmol·L-1 were as model rats. The model rats were randomly divided into model group, rosiglitazone group, and high, middle, low dose of Huangqi Gegen decoction groups(8,4,2 g·kg-1). After intervention by drugs for 8 weeks, FBG, fasting insulin (FINS), leptin, TNF-α level of all rats were measured and insulin sensitivity index(ISI), insulin resistance index(HOMA-IR) were calculated accordingly. At the end of experimental treatment, the total mRNA of greater omental adipose tissues were extracted and the genic fragments of PPAR-γ were amplificated in order to detect their expression levels. Result: Huangqi Gegen decoction could enhance ISI, reduce HOMA-IR, plasm Leptin and TNF-α level in model rats, and increase the expression of PPAR-γ mRNA. Conclution: Huangqi Gegen decoction can improve IR condition of the model rats and its mechanism is probably related to its effect of reducing plasm leptin and TNF-α level,enhancing the genic expressional level of PPAR-γ.