[富含谷胱甘肽的酵母提取物通过激活核因子相关因子2抑制etoh诱导的HepG2细胞铁下垂]。

Yajing Dong, Yanyang Han, Shuqi Ji, Xiaoman Wang, Yan Zhang, Qian Cheng, Hao Han
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引用次数: 0

摘要

目的:研究富谷胱甘肽酵母提取物(GYE)对乙醇(EtOH)诱导的HepG2细胞铁凋亡的改善作用,并进一步探讨其基于调节核因子相关因子2(Nrf2)的可能分子机制。方法:以100 mmol/L EtOH诱导HepG2细胞,以0.1、0.5 mmol/L GYE干预。荧光探针检测细胞内铁~(2+)、脂质过氧化物水平。采用Hoechst/PI染色评估铁下垂的发生。Western blot检测谷胱甘肽过氧化物酶4(GPX4)、重组溶质载体家族7、成员11(SLC7A11)、前列腺素内过氧化物合成酶2(ptgs2)和酰基辅酶a合成酶长链家族4(ACSL4)蛋白的表达。免疫荧光染色检测核易位Nrf2和GPX4的表达。结果:与对照组相比,EtOH组HepG2细胞Fe~(2+)(P<0.05)、胞内脂质过氧化物和铁凋亡(P<0.05)均显著升高。此外,EtOH处理降低了GPX4和SLC7A11的蛋白表达,提高了ACSL4和ptgs2的蛋白表达(P<0.05)。GYE处理显著减轻了乙醚诱导的铁~(2+)积累和脂质过氧化物过量产生(P<0.05)。GYE处理显著抑制etoh诱导的HepG2细胞铁下垂(P<0.05),且高剂量GYE组抑制效果更好。GYE处理显著促进Nrf2核易位(P<0.05)。结论:GYE能有效抑制etoh诱导的HepG2细胞铁凋亡,其分子机制可能与上调Nrf2有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Glutathione-rich yeast extract inhibits EtOH-induced ferroptosis of HepG2 cells by activation of nuclear factorer-related actor 2].

Objective: To investigate the ameliorative effect of glutathione-rich yeast extract(GYE) on ferroptosis of HepG2 cells induced by ethanol(EtOH) and to further explore the potential molecular mechanism based on regulating nuclear factorer-related actor 2(Nrf2).

Methods: HepG2 cells were induced with 100 mmol/L EtOH and intervened by 0.1 and 0.5 mmol/L GYE. The levels of Fe~(2+), lipid peroxides in the cells was detected by fluorescent probe. The occurrence of ferroptosis was assessed by Hoechst/PI staining. The protein expression of glutathione peroxidase 4(GPX4), recombinant solute carrier family 7, member 11(SLC7A11), prostaglandin-endoperoxidesynthase 2(ptgs2)and acyl-CoA synthetase long-chain family 4(ACSL4)were detected by Western blot. Nuclear translocation of Nrf2 and GPX4 expression and were detected by immunofluorescence staining.

Results: Compared with the Control group, the EtOH group showed a significant increase in Fe~(2+)(P<0.05), intracellular lipid peroxides and ferroptosis in HepG2 cells(P<0.05). In addition, EtOH treatment decreased the protein expression of GPX4 and SLC7A11 and increased the protein expression of ACSL4 and ptgs2(P<0.05). GYE treatment significantly mitigated EtOH-induced Fe~(2+) accumulation and overproduction of lipid peroxides(P<0.05). Also, GYE treatment significantly inhibited EtOH-induced ferroptosis of HepG2 cells(P<0.05), and the inhibition effect was better in the high-dose GYE group. GYE treatment significantly promoted nuclear translocation of Nrf2(P<0.05).

Conclusion: GYE can effectively inhibit EtOH-induced ferroptosis in HepG2 cells, and its molecular mechanism may be related to the up-regulating Nrf2.

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