基于氧化应激损伤保护的玉竹多糖降糖活性机制研究  

Antidiabetic Activity Evaluation of POP Based on Its Protection of Oxidative Stress

作　　者：肖作奇 潘涛[1] 邱盼子 欧阳波[1] XIAO Zuoqi;PAN Tao;QIU Panzi;OUYANG Bo(Hunan Provincial Maternal and Child Health Care Hospital, Changsha 410008, China)

机构地区：[1]湖南省妇幼保健院药学制剂部,湖南长沙410008

出　　处：《中医药信息》2021年第5期17-21,共5页Information on Traditional Chinese Medicine

基　　金：湖南省中医药科研计划项目(201996)。

摘　　要：目的:探究玉竹多糖(POP)的降糖活性,初步从氧化应激损伤保护作用方面阐述其改善胰岛素抵抗的作用机制。方法:CCK-8法检测POP对正常和H2O2诱导的氧化应激损伤HepG2细胞活力的影响;随机分成正常对照组、胰岛素抵抗模型组(IR)、罗格列酮组、低剂量POP组和高剂量POP组,探究POP对IR细胞葡萄糖消耗能力的影响;检测POP对IR细胞超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH)水平及PI3K和PPARγ蛋白表达水平的影响。结果:POP对正常培养的HepG2细胞活力没有影响(P>0.05),10 mg/mL POP能显著改善氧化应激损伤细胞的存活率(P<0.05)。POP能显著增加IR细胞的葡萄糖消耗(P<0.05),同时升高SOD和GSH水平(P<0.01),改善MDA蓄积(P<0.01),使IR细胞的PI3K和PPARγ的蛋白表达水平均上调(P<0.05)。结论:POP能改善胰岛素诱导的HepG2细胞的葡萄糖消耗水平,同时会激活胰岛素抵抗细胞氧化应激损伤保护,POP可能通过调节PI3K和PPARγ信号调控通路产生改善IR的生物活性。Objective:To investigate the antidiabetic activity of Polygatum odoratum polysaccharide(POP),and to elaborate its mechanism in improving insulin resistance(IR)in terms of protecting the damage of oxidative stress(OS).Methods:CCK-8 assay kit was used to detect the influence of POP on the activity of HepG2 cells under normal state and H2O2-induced OS state.Cells were divided into the normal control group,the IR group,the model group,the Rosiglitazone group,the low-dose POP group and the high-dose POP group.Superoxide dismutase(SOD),malondialdehyde(MDA)and glutathione peroxidase(GSH)were detected,the expressions of PI3K and PPARγwere analyzed after being cultured with POP.Results:POP had no influence to the cell viability of HepG2 under normal state(P>0.05),and 10 mg/mL POP could significantly improve the viability of H2O2-induced OS HepG2(P<0.05).POP could significantly increase the glucose consumption of IR cells(P<0.05),increase the levels of SOD and GSH(P<0.01),and decrease the MDA in IR cells(P<0.01).After POP incubation,the protein expression levels of PI3K and PPARγwere up-regulated in IR cells(P<0.05).Conclusion:POP can ameliorate the glucose consumption level of insulin-induced HepG2 cells by protecting the IR cells from OS,POP is involved in activating PI3K and PPARγsignaling pathway in IR.

关 键 词：玉竹多糖 胰岛素抵抗 氧化应激 PI3K PPARΓ 

分 类 号：R285.5[医药卫生—中药学]