太子参多糖减轻高脂诱导的小鼠肝脏胰岛素抵抗  

Radix Pseudostellariae polysaccharide attenuates high fat diet induced hepatic insulin resistance in mice

作　　者：王琪[1] 柴单单 吴晓华 任丽伟[3] 刘永年[1] 于志文[3] 

机构地区：[1]青海大学医学院病理生理学教研组,青海西宁810000 [2]福建省闽东力捷迅药业有限公司研发部,福建宁德352000 [3]福建中医药大学生物医药研发中心,福建福州350000

出　　处：《中国病理生理杂志》2015年第4期685-689,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81270886)

摘　　要：目的:通过研究太子参多糖(Radix Pseudostellariae polysaccharide,RPP)减轻高脂肪诱导肝脏胰岛素抵抗的作用,探寻其主要影响因素及发生的分子机制。方法:随机将C57BL/6J小鼠分为低脂饲料对照组(LFD组)和高脂饲料组(HFD组),16周后,经腹腔注射丙酮酸耐量试验(IPPTT)确定胰岛素抵抗糖代谢紊乱模型成功后,开始进行含RPP(500 mg/kg)的高脂饲料干预(HFD+RPP组),连续干预4周之后,检测丙酮酸耐量以及肝脏组织和线粒体丙二醛(MDA)含量。同时采用Western blot法检测肝脏组织中p-AKT(Ser473/Thr308)、p-AMPK、核因子E2相关因子2(Nrf2)、NQO1和IκBα的蛋白水平变化。结果:经RPP干预后,模型组小鼠血糖水平明显降低;肝脏和线粒体的MDA水平显著降低;肝脏组织p-AKT及p-AMPK的蛋白水平明显增高;NQO1、HO-1和IκBα蛋白水平也同时上调。结论:太子参多糖能够有效抑制高脂肪诱导的C57BL/6J小鼠高血糖作用,其机制可能与改善肝脏胰岛素信号转导,并减轻氧化应激反应,同时激活Nrf2信号通路及抑制肝脏炎症信号激活作用有关。AIM：To study the role of Radix Pseudostellariae polysaccharide （ RPP） in hepatic insulin resist-ance.METHODS：Six-week-old C57BL/6J mice were randomly divided into low-fat diet （LFD） control group and high-fat diet （ HFD） model group.After 16 weeks, intraperitoneal pyruvate tolerance test （ IPPTT） was performed to determine the establishment of the HFD-induced hepatic insulin resistance model.HFD containing RPP （500 mg/kg） was given for 4 consecutive weeks.IPPTT, liver malondialdehyde （ MDA） level and liver mitochondrial MDA level were measured.The protein levels of p-AKT （Ser473/Thr308）, p-AMPK, nuclear factor E2-related factor 2 （Nrf2）, NQO1 and IκBαin the liver tissues were measured by Western blot.RESULTS：After administration of RPP, a significant reduction in the levels of blood glucose and hepatic mitochondrial MDA was observed.The levels of p-AKT （ Ser473/Thr308） and p-AMPK were significantly elevated in the liver tissues.The hepatic IκBαlevels were up-regulated.RPP also enhanced the expression of Nrf2 system-regulated proteins NQO1 and HO-1 in the liver tissues.CONCLUSION：Radix Pseudostellariae polysaccha-rides effectively reduce HFD-induced hepatic insulin resistance in C57BL/6J mice and improves liver glucose metabolism by ameliorating HFD-impaired hepatic transduction of insulin signaling, activating Nrf2-associated signaling and inhibiting the expression of inflammatory signaling proteins.

关 键 词：C57BL/6J小鼠 胰岛素抵抗 太子参多糖 氧化应激 丙二醛 

分 类 号：R363[医药卫生—病理学]