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中国应用生理学杂志 ›› 2017, Vol. 33 ›› Issue (6): 568-571.doi: 10.12047/j.cjap.5601.2017.134

• 研究论文 • 上一篇    下一篇

枸杞多糖对HepG2细胞胰岛素抵抗的改善作用及机制研究

许拓1, 凌宏艳1, 龙佳2, 何剑琴1, 杨丝丝1, 朱责梅1, 颜灿群2, 奉水东3   

  1. 1. 南华大学生理学教研室, 湖南 衡阳 421001;
    2. 南华大学附属第二医院内分泌科, 湖南 衡阳 421001;
    3. 南华大学社会医学与卫生事业管理学教研室, 湖南 衡阳 421001
  • 收稿日期:2016-11-21 修回日期:2017-06-29 出版日期:2017-11-28 发布日期:2018-06-19
  • 基金资助:
    教育部留学归国基金(教外司留[2014]1685号);湖南教育厅(16C1411);衡阳市科技局(2016KJ64)

Ameliorative effects and the mechanism of lyceum barbarum polysaccharide on insulin resistance of HepG2 cell

XU Tuo1, LING Hong-yan1, LONG Jia2, HE Jian-qin1, YANG Si-si1, ZHU Ze-mei1, YAN Can-qun2, FENG Shui-dong3   

  1. 1. Department of Physiology, University of South China, Hengyang 421001, China;
    2. The Second Hospital of University of South China, University of South China, Hengyang 421001, China;
    3. Department of Social Medicine and Health Service Management, University of South China, Hengyang 421001, China
  • Received:2016-11-21 Revised:2017-06-29 Online:2017-11-28 Published:2018-06-19
  • Contact: 奉水东,Tel:86-0734-8281621;E-mail:shuidong_f@hotmail.com E-mail:shuidong_f@hotmail.com
  • Supported by:
    教育部留学归国基金(教外司留[2014]1685号);湖南教育厅(16C1411);衡阳市科技局(2016KJ64)

摘要: 目的:观察不同浓度的枸杞多糖(LBP)对HepG2细胞胰岛素抵抗的影响并探讨其机制。方法:采用高糖高胰岛素处理HepG2细胞24 h建立胰岛素抵抗细胞模型后,用台盼蓝检测活力大于95%的HepG2细胞,以104/孔密度接种于96孔板内,细胞贴壁后以30 μg/ml、100 μg/ml、300 μg/ml的LBP培养48 h,200 μl/well,各组均设4个复孔。检测不同浓度的LBP对HepG2细胞活性及胰岛素抵抗的影响;细胞内丙二醛(MDA)含量和超氧化物歧化酶(SOD)的活性;各组细胞胰岛素信号转导通路中相关蛋白(IRS-2、PI3-K、Akt、GLUT2)的表达。结果:MTT显示:与正常对照组相比,IR模型组MDA含量显著升高,SOD活力明显降低,同时IRS-2、PI-3K、Akt、GLUT2蛋白表达水平明显下降;与IR模型组相比,中、高浓度LBP组MDA的含量明显降低,SOD的活力显著升高,且IRS-2、PI-3K、Akt、GLUT2蛋白表达水平明显升高;在相同的时间内,随着LBP浓度的增加,OD值逐渐降低;在同一浓度干预下,随着时间的延长,OD值也逐渐降低;葡萄糖消耗实验表明中、高浓度的LBP可显著提高胰岛素抵抗HepG2细胞的葡萄糖消耗量,而低浓度LBP对HepG2细胞葡萄糖消耗量无明显影响。结论:中、高浓度枸杞多糖能改善HepG2细胞胰岛素抵抗,其作用机制可能与降低细胞氧化应激水平及提高胰岛素信号传导通路相关蛋白表达有关。

关键词: 枸杞多糖, HepG2细胞, 胰岛素抵抗, 氧化应激, 胰岛素信号通路

Abstract: Objective: To observe the effects of lyceum barbarum polysaccharide (LBP) on insulin resistance of HepG2 cells and investigate its possible mechanism.Methods: IR-HepG2 cell model was induced with high glucose and high insulin in combination for 24 hours,with 104/vaccination in the 96-well plates, hole density after adherent cells (30 μg/ml、100 μg/ml、300 μg/ml) LBP cultivate 48 h, 200 μl/hole, each all had four holes. The effects of LBP at different concentrations on HepG2 cell activity and insulin resistance were tested. Intracellular malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were detected. The expressions of related proteins in insulin signal transduction pathways such as insulin receptor substrate-2(IRS-2), phosphatidylinositol-3-kinase(PI3-K), protein kinase B(Akt) and glucose transport-2(GLUT2) were determined.Results: Compared with normal control group, the content of MDA was increased significantly and the activity of SOD and the expression levels of IRS-2,PI-3K,Akt and GLUT2 were decreased significantly in the IR model group. Compared with IR model group, medium and high concentrations of LBP decreased the content of MDA and increased the activity of SOD and the expression levels of IRS-2, PI-3K, Akt and GLUT2 in insulin-resistant HepG2 cells. MTT showed that at the same time, the OD value gradually decreased with the increase of LBP's concentration; under the same concentration of LBP, the OD value also gradually decreased with the extension of time, which indicated that LBP inhibited the proliferation of HepG2 cells with time and concentration-dependent manner. Glucose consumption experiment indicated that medium and high concentration of LBP could increase the glucose consumption of insulin-resistant HepG2 cells significantly, but low concentration of LBP had no significant impacted on glucose consumption of insulin-resistant HepG2 cells.Conclusion: Medium and high concentration of LBP can improve insulin resistance of HepG2 cell, its mechanisns may be associated with decreasing the level of oxidative stress and increasing the protein expressions of insulin signaling pathway.

Key words: lyceum barbarum polysaccharide, HepG2 cell, insulin resistance, oxidative stress, insulin signaling pathway

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