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作 者:李国生[1] 刘栩晗[2] 黄澜[1] 朱华[1] 刘亚莉[1] 马春梅[1]
机构地区:[1]大连医科大学附属第一医院,辽宁大连116011 [2]辽宁省大连市中心医院,辽宁大连116003
出 处:《现代中西医结合杂志》2011年第17期2099-2103,共5页Modern Journal of Integrated Traditional Chinese and Western Medicine
摘 要:目的研究黄连素对2型糖尿病中国地鼠肝脏肝X受体(LXR)及其靶基因表达的影响,探讨黄连素治疗肝脏脂诱性胰岛素抵抗的分子机制。方法以高脂饮食及结合小剂量链脲菌素的方法建立胰岛素抵抗和2型糖尿病中国地鼠模型。成模后随机分成正常对照组、胰岛素抵抗组、2型糖尿病组和黄连素治疗组,治疗9周。应用实时定量PCR方法检测各组地鼠肝脏LXR s及其靶基因的表达。结果模型地鼠脂肪变的肝脏中LXRα、胆固醇7α羟化酶1(CYP7A1)和葡萄糖激酶(Gck)的表达降低,磷酸烯醇式丙酮酸羧激酶(PEPCK)、葡萄糖-6-磷酸酶(G6Pase)和过氧化物酶体增殖体激活的受体γ共激活因子-1α(PGC-1α)的表达升高,而LXRβ的表达未改变。黄连素有效地改善胰岛素抵抗,同时逆转了LXRα及其靶基因表达的改变而未影响LXRβ的表达。结论 LXRα及其靶基因参与黄连素治疗2型糖尿病地鼠脂诱性胰岛素抵抗的分子机制。Objective It is to study the influences of berberine on the expression of hepatic X receptors(LXRs) and their target genes in liver of Chinese hamsters with type 2 diabetes mellitus(T2DM) and approach the molecular mechanisms of berberine on fat-induced hepatic insulin resistance.Methods The insulin-resistant and T2DM Chinese hamster models were induced by high-fat diet without or with low-dose streptozotocin.After the induction of hamster models,the hamsters were randomly divided into four groups: normal control group,insulin-resistant group,T2DM group and berberine-treated groups.After nine-week treatment,the expression of hepatic LXRs and their target genes from different groups were detected with real-time RT-PCR.Results The expressions of LXRα,cholesterol 7alpha-hydroxylase(CYP7A1) and glucokinase(Gck) were lowered and the expressions of phosphoenolpyruvate carboxykinase(PEPCK),glucose-6-phosphatase(G6Pase) and peroxisome proliferator-activated receptor γ coactivator-1α(PGC-1α) were heightened in fatty liver of hamster models.The expression of LXRβ was unchanged.Berberine effectively improved insulin resistance,reversed the altered expression of LXRα and its target genes in diabetic hamsters and unaffected the expression of LXRβ.Conclusion LXRα and its target genes participate in the molecular mechanisms of berberine on fat-induced insulin resistance in T2DM hamsters.
关 键 词:黄连素 2型糖尿病 肝X受体 胰岛素抵抗 中国地鼠 肝脏
分 类 号:R332[医药卫生—人体生理学]
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