食品工业科技2024,Vol.45Issue(20):369-377,9.DOI:10.13386/j.issn1002-0306.2023120297
20-羟基蜕皮激素对高糖诱导HepG2细胞氧化损伤的作用及机制研究
Role and Mechanism of 20-Hydroxyecdysone in Oxidative Damage of HepG2 Cells Induced by High Glucose
摘要
Abstract
Objective:To explore the protective effects of 20-Hydroxyecdysone(20-HE)on high glucose induced HepG2 cells and its related molecular mechanism.Methods:In this study,high glucose(50 mmol/L glucose)was used to establish the oxidative damage model in HepG2 cells.The CCK-8 assay,caspase-3 assay,fluorescent probe method,and colorimetric method were used to assess the levels of cell viability,apoptosis,oxygen species(ROS),superoxide dismutase(SOD),catalase(CAT),and malondialdehyde(MDA),respectively.The signaling pathways involved in the regulation of 20-HE were predicted using bioinformatics analysis.The phosphorylation level of Akt protein was detected by Western blot to evaluate the activation level of the PI3K/Akt signaling pathway.The involvement of the PI3K/Akt signaling pathway in the regulatory effects of 20-HE was verified using the inhibitor LY294002.Results:Treatment with 20-HE had no significant toxic effect on HepG2 cells at concentrations lower than 20 μmol/L.In the injured cells,20-HE could significantly improve the viability(P<0.05),inhibit the apoptosis(P<0.05),down-regulate the level of ROS,improve the levels of SOD and CAT(P<0.05),and down-regulate the level of MDA(P<0.05).PI3K/Akt signaling pathway was the potential downstream mechanism of regulatory effects exerted by 20-HE.20-HE could significantly up-regulate the level of PI3K/Akt signaling pathway in the injured cells(P<0.05).LY294002 could reverse the protective effects exerted by 20-HE on the injured cells.Conclusion:20-HE exerted protective effects on high glucose induced oxidative damage in HepG2 cells by activating the PI3K/Akt signaling pathway.关键词
20-羟基蜕皮激素/高糖/HepG2细胞/氧化应激/PI3K/Akt信号通路Key words
20-hydroxyecdysone/high glucose/HepG2 cells/oxidative stress/PI3K/Akt signaling pathway分类
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王梦媛,刘咸筠,孟祥龙,李皓,李占东,殷玉和..20-羟基蜕皮激素对高糖诱导HepG2细胞氧化损伤的作用及机制研究[J].食品工业科技,2024,45(20):369-377,9.基金项目
吉林省科技发展计划项目(20210202059NC,20220202076NC,20220202088NC). (20210202059NC,20220202076NC,20220202088NC)