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预防医学  2020, Vol. 32 Issue (2): 121-124    DOI: 10.19485/j.cnki.issn2096-5087.2020.02.004
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黄芪多糖缓解HepG2细胞胰岛素抵抗模型的分子机制研究
程玥, 毛竹君, 张芯, 夏旭芬
浙江省立同德医院检验科,浙江 杭州 310012
Molecular mechanism of astragalus polysaccharide in alleviating insulin resistance in HepG2 cells
CHENG Yue, MAO Zhujun, ZHANG Xin, XIA Xufen
Department of Endocrinology,Tongde Hospital of Zhejiang Province,Hangzhou,Zhejiang 310012,China
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摘要 目的 观察黄芪多糖(AP)对HepG2细胞胰岛素抵抗模型的影响,从脂质代谢和氧化应激方面探讨其作用的分子机制。方法 HepG2细胞分为3组:对照组不进行干预处理;模型组加入200 μL含胰岛素终浓度为10-6 mol/L的细胞完全培养基,孵育48 h,建立胰岛素抵抗模型;AP组HepG2细胞胰岛素抵抗模型中加入最适浓度 AP。24 h后,采用分光光度法检测3组细胞中H2O2浓度,采用RT-PCR法检测过氧化物酶体增殖剂激活受体γ(PPARγ)的mRNA相对表达量。结果 AP可提高胰岛素抵抗模型中HepG2细胞存活率,呈一定的剂量依赖性,AP浓度为10 μM时Hep G2细胞的存活率最高,为(118.26±1.17)%。AP组、模型组和对照组HepG2细胞内H2O2浓度分别为(0.82±0.09)μM、(1.30±0.16)μM和(0.78±0.09)μM,AP组HepG2细胞中H2O2浓度较模型组降低(P<0.05),与对照组差异无统计学意义(P>0.05)。AP组、模型组和对照组HepG2细胞中PPARγ的mRNA相对表达量分别为0.96±0.04、0.51±0.05和1.00±0.11,AP组HepG2细胞中PPARγ的mRNA相对表达量较模型组升高(P<0.05),与对照组差异无统计学意义(P>0.05)。结论 在体外胰岛素抵抗模型中,AP能提高细胞存活率,降低细胞内H2O2浓度,增加PPARγ表达;AP可能影响脂质代谢途径以改善胰岛素抗体。
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关键词 黄芪多糖HepG2细胞胰岛素抵抗氧化应激    
AbstractObjective To clarify the effect of astragalus polysaccharide (AP) on insulin resistance model of HepG2 cells induced by hyperinsulinemia and its underlying molecular mechanism in lipid metabolism and oxidative stress. Methods HepG2 cells were divided into three groups: the control group was treated without any intervention; the model group was treated with 200 μL cell culture medium containing 10-6 mol/L insulin for 48 hours to build an insulin resistance model; the AP group was treated with optimal concentration of AP based on an insulin resistance model. After 24 hours, the concentration of H2O2 and the expression of PPARγ in each group were detected. Results AP could improve the survival rate of insulin-resistant HepG2 cells in a dose-dependent manner. The highest survival rate of the cells was (118.26±1.17)% with 10 μM AP. The concentration of H2O2 in the AP group was (0.82±0.09) μM, which was lower than (1.30±0.16) μM in the model group (P<0.05), but was close to (0.78±0.09) μM in the control group (P>0.05). The relative mRNA expression of PPARγ in the AP group was 0.96±0.04, which was higher than 0.51±0.05 in the model group (P<0.05), but was close to 1.00±0.11 in the control group (P>0.05). Conclusions In the insulin resistance model in vitro, AP can significantly increase the cell survival rate, reduce intracellular H2O2 concentration, and promote the expression of PPARγ. The mechanism may be related to lipid metabolism.
Key wordsastragalus polysaccharide    HepG2 cell    insulin resistance    oxidative stress
收稿日期: 2019-09-26      出版日期: 2020-02-27
ZTFLH:  R587.1  
基金资助:国家自然科学基金(81603351)
作者简介: 夏旭芬,E-mail:823676828@qq.com
引用本文:   
程玥, 毛竹君, 张芯, 夏旭芬. 黄芪多糖缓解HepG2细胞胰岛素抵抗模型的分子机制研究[J]. 预防医学, 2020, 32(2): 121-124.
CHENG Yue, MAO Zhujun, ZHANG Xin, XIA Xufen. Molecular mechanism of astragalus polysaccharide in alleviating insulin resistance in HepG2 cells. Preventive Medicine, 2020, 32(2): 121-124.
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http://www.zjyfyxzz.com/CN/10.19485/j.cnki.issn2096-5087.2020.02.004      或      http://www.zjyfyxzz.com/CN/Y2020/V32/I2/121
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