Yajing Dong, Yanyang Han, Shuqi Ji, Xiaoman Wang, Yan Zhang, Qian Cheng, Hao Han
{"title":"[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]。","authors":"Yajing Dong, Yanyang Han, Shuqi Ji, Xiaoman Wang, Yan Zhang, Qian Cheng, Hao Han","doi":"10.19813/j.cnki.weishengyanjiu.2025.02.015","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>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).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>GYE can effectively inhibit EtOH-induced ferroptosis in HepG2 cells, and its molecular mechanism may be related to the up-regulating Nrf2.</p>","PeriodicalId":57744,"journal":{"name":"卫生研究","volume":"54 2","pages":"273-300"},"PeriodicalIF":0.0000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Glutathione-rich yeast extract inhibits EtOH-induced ferroptosis of HepG2 cells by activation of nuclear factorer-related actor 2].\",\"authors\":\"Yajing Dong, Yanyang Han, Shuqi Ji, Xiaoman Wang, Yan Zhang, Qian Cheng, Hao Han\",\"doi\":\"10.19813/j.cnki.weishengyanjiu.2025.02.015\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>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).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>GYE can effectively inhibit EtOH-induced ferroptosis in HepG2 cells, and its molecular mechanism may be related to the up-regulating Nrf2.</p>\",\"PeriodicalId\":57744,\"journal\":{\"name\":\"卫生研究\",\"volume\":\"54 2\",\"pages\":\"273-300\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"卫生研究\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.19813/j.cnki.weishengyanjiu.2025.02.015\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"卫生研究","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.19813/j.cnki.weishengyanjiu.2025.02.015","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
[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.