中国医科大学学报2025，Vol.54Issue(4)：295-300,6.DOI:10.12007/j.issn.0258-4646.2025.04.002
银杏黄酮苷介导NR4A2/p53/Bax通路调控自噬抑制心肌细胞凋亡
Ginkgetin mediates the NR4A2/p53/Bax pathway to regulate autophagy and inhibit cardiomyocyte apoptosis
摘要
Abstract
Objective To investigate the mechanism by which ginkgetin attenuates H9c2 cells injury.Methods H9c2 cells were divided into five groups:control,lipopolysaccharide(LPS),LPS+3-methyladenine(3-MA,an autophagy inhibitor),LPS+ginkgetin,and LPS+3-MA+ginkgetin.Cell viability and cytotoxicity were assessed using the cell CCK-8 and lactate dehydrogenase assays,respectively.Immunofluorescence staining for LC3,monodansylcadaverine staining for autophagosomes,and flow cytometry were used to measure apop-tosis rates.Quantitative real-time PCR was performed to measure the expression of NR4A2/p53/Bax pathway.Western blotting was used to detect the expression of NR4A2,p53,Bax,LC3,Beclin-1,p62,cleaved caspase-3,and Bcl-2 proteins.Results Compared to the LPS group,ginkgetin significantly increased LC3 fluorescence levels and monodansylcadaverine fluorescence intensity,decreased apoptosis,upregulated NR4A2,downregulated p53 and Bax,increased LC3,Beclin-1,and Bcl-2 proteins,and decreased p62 and cleaved caspase-3(P＜0.05).The autophagic inhibitor,3-MA,confirmed that ginkgetin protected H9c2 cells from LPS-induced apoptosis via autophagy regulation.Conclusion Ginkgetin mitigated cardiomyocyte injury by enhancing autophagic flux and alleviating LPS-induced H9c2 cells apoptosis by modulating the NR4A2/p53/Bax pathway.关键词
银杏黄酮苷/H9c2细胞/自噬/细胞凋亡Key words
ginkgetin/H9c2 cell/autophagy/apoptosis分类
医药卫生引用本文复制引用
李涵,魏东升,曹慧敏,吴欣悦,韩叶蕾,张哲..银杏黄酮苷介导NR4A2/p53/Bax通路调控自噬抑制心肌细胞凋亡[J].中国医科大学学报,2025,54(4):295-300,6.基金项目
国家中医药管理局青年岐黄学者支持项目(20201A2180) （20201A2180）
辽宁省科技计划联合计划(基金)项目(2023-MSLH-191) （基金）
