安徽医科大学学报2026，Vol.61Issue(4)：636-643,8.DOI:10.19405/j.cnki.issn1000-1492.2026.04.007
金雀异黄酮对依托泊苷诱导软骨细胞衰老的保护作用及其机制
Protective effect and mechanism of genistein on etoposide-induced chondrocyte senescence
摘要
Abstract
Objective To investigate the protective effect of genistein(Gen)on etoposide-induced chondrocyte se-nescence and its underlying mechanism.Methods The C28/I2 cell line was treated with different concentrations of Gen and etoposide,and the cell viability was detected by the CCK-8 assay.The senescence model of C28/I2 chondrocytes was induced by etoposide,with Gen intervention.Senescence-associated β-galactosidase(SA-β-gal)staining was performed to detect the senescence-positive rate and staining characteristics of chondrocytes.The ex-pressions of peroxiredoxin 6(Prdx6),cyclin-dependent kinaseto clarify the functional necessity of Prdx6.Results Compared with the etoposide group,the C28/I2 chondrocyte viability significantly increased(P<0.01),the expres-sion ofsenescence-associated proteins p21 and p16 decreased(P<0.01,P<0.05),the expression of senescence-associated genes p21 and p16 reduced(both P<0.01),the fluorescence intensity of senescence-associated proteins p21 and p16 was diminished(P<0.05,P<0.01),and the proportion of SA-β-gal-positive cells decreased(P<0.01)in the Gen+etoposide group.Compared with the Control group,the expression of Prdx6 was downregulated in the etoposide group(P<0.05).Compared with the etoposide group,the expression of Prdx6 was upregulated in the Gen+etoposide group(P<0.01).Compared with the Control group,the GPx activity significantly decreased in the si-Prdx6 group(P<0.01).Furthermore,compared with the si-Prdx6 group,the GPx activity increased in the si-Prdx6+Gen group(P<0.05).Molecular docking results revealed that Gen formed hydrogen bond interactions with the active site of Prdx6.After Prdx6 knockdown,the expression of senescence-associated genes p21 and p16 and the fluorescence intensity of senescence-associated proteins p21 and p16 both increased in the Gen+etoposide+si-Prdx6 group(both P<0.01).Conclusion Gen can inhibit etoposide-induced senescence of C28/I2 chondro-cytes by upregulating the expression of Prdx6.This study provides potential drug targets and experimental basis for the prevention and treatment of chondrocyte senescence-related diseases.关键词
金雀异黄酮/Prdx6/软骨细胞/衰老/分子对接/依托泊苷Key words
genistein/Prdx6/chondrocytes/senescence/molecular docking/etoposide分类
医药卫生引用本文复制引用
王金虹,陈天宇,毛丽芳,赵英杰,周仁鹏,胡伟,鲁超..金雀异黄酮对依托泊苷诱导软骨细胞衰老的保护作用及其机制[J].安徽医科大学学报,2026,61(4):636-643,8.基金项目
安徽省卫生健康科研项目(编号:AHWJ2024Aa40016) （编号:AHWJ2024Aa40016）
合肥综合性国家科学中心大健康研究院职业医学与健康联合研究中心开放基金项目(编号:OMH-2023-03) （编号:OMH-2023-03）
安徽自然科学基金项目(编号:2208085MH215) （编号:2208085MH215）
安徽省中医药传承创新科研项目(编号:2020cczd05) Health Research Project of Anhui Province(No.AHWJ2024Aa40016) （编号:2020cczd05）
Occupational Medi-cine and Health Joint Research Project from Institute of Health and Medicine,Hefei Comprehensive National Sci-ence Center(No.OMH-2023-03) （No.OMH-2023-03）
Natural Science Foundation of Anhui Province(No.2208085MH215) （No.2208085MH215）
Scien-tific Research Project of Inheritance and Innovation of Traditional Chinese Medicine in Anhui Province.(No.2020cczd05) （No.2020cczd05）
