猫棒束孢对IR-Hep G2细胞氧化应激的改善作用及机制  

Ameliorative effect and mechanism of Isaria felina on oxidative stress insulin resistance of Hep G2 cells

作　　者：陈静静 陈丽霞[2] 赵莉莉[2] 杨永明[2] 杨喜花[1,2] CHEN Jingjing;CHEN Lixia;ZHAO Lili;YANG Yongming;YANG Xihua(School of Public Health,Shanxi Medical University,Taiyuan 030001,China;Experimental Animal Center,The Affiliated Cancer Hospital of Shanxi Medical University,Taiyuan 030013,China)

机构地区：[1]山西医科大学公共卫生学院,山西太原030001 [2]山西医科大学附属肿瘤医院实验动物中心,山西太原030013

出　　处：《西部医学》2023年第2期172-175,181,共5页Medical Journal of West China

基　　金：山西省卫生健康委员会科研课题(2021072)。

摘　　要：目的探讨猫棒束孢(IF)对胰岛素抵抗Hep G2(IR-HepG2)细胞氧化应激的保护作用及其机制。方法MTT法测定不同浓度IF和胰岛素对Hep G2细胞增殖的影响,用含10-8 mol·L^(-1)胰岛素的高糖DMEM培养基诱导Hep G2细胞48 h,建立Hep G2细胞胰岛素抵抗模型。采用试剂盒测定葡萄糖消耗量、超氧化物歧化酶(SOD)、丙二醛(MDA)、胰岛素受体底物1(IRS-1)、磷脂酰肌醇-3-羟基酶(PI3K)、蛋白激酶B(Akt)的含量。结果在IF浓度为5μg·mL^(-1)和10μg·mL^(-1)对细胞生长无显著促进作用,故浓度选用于5μg·mL^(-1)和10μg·mL^(-1);胰岛素处理48 h后只有10-8 mol·L^(-1)剂量组对照细胞生长无显著抑制作用,故选用胰岛素浓度为10-8 mol·L^(-1),培养48 h建立胰岛素抵抗模型。与正常组比较,模型组IR-Hep G2细胞葡萄糖消耗量显著下降(P<0.01);与模型组比较,各浓度猫棒束孢干预后的IR-Hep G2细胞的葡萄糖消耗量显著上升(P<0.01)。与正常组比较,模型组Hep G2细胞的SOD含量显著下降(P<0.01),MDA含量显著上升(P<0.01),IRS-1、PI3K、Akt的含量显著下降(P<0.05)。经IF处理后SOD含量显著提高(P<0.01),MDA含量显著降低(P<0.01),IRS-1、PI3K、Akt的含量显著升高(P<0.01、P<0.05、P<0.01)。结论IF能够改善胰岛素抵抗Hep G2细胞模型的糖代谢和氧化应激水平,并通过调控IRS-1/PI3K/Akt信号通路起到改善胰岛素抵抗的作用。Objective To establish an insulin-resistant Hep G2 cell model and observe the protective effect and mechanism of Isaria feline(IF)on oxidative stress of insulin-resistant Hep G2 cells.Methods The proliferation of Hep G2 cells was determined by MTT assay.Hep G2 cells were induced by high-glucose DMEM medium containing 10-8 mol·L^(-1)insulin for 48 h to establish insulin-resistant Hep G2 cell model.Glucose residue,superoxide dismutase(SOD),malondialdehyde(MDA),IRS-1,PI3K and Akt were determined by kit.Results The concentration of 5μg·mL^(-1)and 10μg·mL^(-1)of IF did not significantly promote the cell growth,and the insulin concentration was 10-8 mol·L and cultured for 48h to establish the insulin resistance model.Compared with normal group,the glucose consumption of Hep G2 cells in model group decreased significantly(P<0.01),SOD content decreased significantly(P<0.01),MDA content increased significantly(P<0.01),the content of IRS-1,PI3K and Akt decreased significantly(P<0.01,P<0.01,P<0.05).After treatment,glucose consumption was increased significantly(P<0.01),SOD content increased significantly(P<0.01),MDA content decreased significantly(P<0.01),the content of IRS-1、PI3K and Akt were increased significantly(P<0.01,P<0.05,P<0.01).Conclusion IF can improve glucose metabolism and oxidative stress levels in insulin-resistant Hep G2 cell model,and alleviates insulin resistance by regulating IRS-1/PI3K/Akt signaling pathway.

关 键 词：猫棒束孢 胰岛素抵抗 Hep G2细胞 氧化应激 胰岛素信号通路 

分 类 号：R285.5[医药卫生—中药学]