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中国精品科技期刊2020
王梦媛,刘咸筠,孟祥龙,等. 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. doi: 10.13386/j.issn1002-0306.2023120297.
引用本文: 王梦媛,刘咸筠,孟祥龙,等. 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. doi: 10.13386/j.issn1002-0306.2023120297.
WANG Mengyuan, LIU Xianjun, MENG Xianglong, et al. Role and Mechanism of 20-Hydroxyecdysone in Oxidative Damage of HepG2 Cells Induced by High Glucose[J]. Science and Technology of Food Industry, 2024, 45(20): 369−377. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2023120297.
Citation: WANG Mengyuan, LIU Xianjun, MENG Xianglong, et al. Role and Mechanism of 20-Hydroxyecdysone in Oxidative Damage of HepG2 Cells Induced by High Glucose[J]. Science and Technology of Food Industry, 2024, 45(20): 369−377. (in Chinese with English abstract). 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: 目的:探究20-羟基蜕皮激素(20-Hydroxyecdysone,20-HE)对高糖诱导HepG2细胞氧化损伤的保护作用及相关分子机制。方法:利用高糖(50 mmol/L葡萄糖)建立HepG2细胞氧化损伤模型,分别采用CCK-8法、caspase-3活性检测实验、荧光探针法和比色法检测细胞的活力、凋亡、活性氧(Reactive Oxygen Specie,ROS)、超氧化物歧化酶(Superoxide Dismutase,SOD)、过氧化氢酶(Catalase,CAT)和丙二醛(Malondialdehyde,MDA)的水平。基于生物信息学分析的方法对参与20-HE调控作用的相关信号通路进行预测,采用Western blot检测Akt蛋白的磷酸化水平,评价PI3K/Akt信号通路的激活水平,利用PI3K/Akt信号通路的抑制剂(LY294002)验证其是否参与20-HE发挥的调控作用。结果:20-HE的浓度低于20 μmol/L对HepG2细胞没有显著毒性作用;20-HE可以显著提高损伤细胞的活力(P<0.05),显著抑制损伤细胞的凋亡(P<0.05),显著下调损伤细胞的ROS水平(P<0.05),显著提高SOD和CAT的水平(P<0.05),显著下调MDA水平(P<0.05);PI3K/Akt信号通路是20-HE发挥调控作用的潜在下游机制;20-HE可以显著上调损伤细胞中PI3K/Akt信号通路的水平(P<0.05);LY294002可以逆转20-HE对损伤细胞发挥的保护作用。结论:20-HE通过激活PI3K/Akt信号通路发挥对高糖诱导HepG2细胞氧化损伤的保护作用。

     

    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.

     

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