中医药信息2025，Vol.42Issue(9)：27-35,9.DOI:10.19656/j.cnki.1002-2406.20250905
基于Nrf2/HO-1通路介导的细胞铁死亡探究牡荆素对鼻咽癌细胞的作用机制研究
Study on the Mechanism of Vitexin's Effect on Nasopharyngeal Carcinoma Cells Mediated by the Nrf2/HO-1 Pathway-Regulated Ferroptosis
摘要
Abstract
Objective:To investigate the effect of vitexin(VT)on nasopharyngeal carcinoma cells and its relationship with ferroptosis mediated by the Nrf2/HO-1 pathway.Methods:Nasopharyngeal carcinoma cells were treated with different concentrations of VT(0,5,10,25,50,100,200 μmol/L),and cell viability was detected.CNE-2 cells were randomly divided into control group,VT-H+Nrf2 agonist group,and VT low(VT-L),medium(VT-M),and high(VT-H)dose groups.After 24 h of drug intervention,cell proliferation was detected by EdU assay;cell migration and invasion were detected by Transwell assay;mitochondrial morphological changes were observed by transmission electron microscopy;oxidative stress indicators and iron ion levels were detected by assay kits;and protein expressions of ferroptosis and the Nrf2/HO-1 pathway were detected by Western blot.A subcutaneous xenograft tumor model of nasopharyngeal carcinoma was established in nude mice and divided into Control group,VT-L group,VT-M group,and VT-H group.After drug intervention,tumor weight and volume were measured;histopathological changes in tumor tissues were observed by HE staining;oxidative stress indicators and iron ion levels in tumor tissues were detected by assay kits;mitochondrial morphological changes were observed by transmission electron microscopy;and protein expressions of ferroptosis and the Nrf2/HO-1 pathway in tumor tissues were detected by Western blot.Results:With increasing VT concentrations,the viability of nasopharyngeal carcinoma cells gradually decreased(P<0.05).CNE-2 cells were selected for further study,and VT concentrations of 25,50,and 100 μmol/L were used for subsequent experiments.Compared with the Control group,all VT dose groups showed significantly reduced EdU proliferation,migration and invasion abilities,GSH content,and protein expressions of Nrf2,GPX4,and SLC7A11(P<0.05),while ROS,Fe2+,MDA levels,and ACSL4 protein expression were significantly increased(P<0.05),with mitochondria exhibiting typical ferroptosis features.Compared with the VT-H group,the VT-H+Nrf2 agonist group showed significantly increased EdU proliferation,migration and invasion abilities,GSH content,and protein expressions of Nrf2,GPX4,and SLC7A11(P<0.05),while ROS,Fe2+,MDA levels,and ACSL4 protein expression were significantly decreased(P<0.05),with alleviated mitochondrial damage.VT inhibited the growth of subcutaneous xenograft tumors in nude mice,downregulated Nrf2/HO-1 pathway protein expression,and induced ferroptosis.Conclusion:VT inhibits proliferation,migration,and invasion of nasopharyngeal carcinoma cells by inducing ferroptosis,and its mechanism is related to the inhibition of the Nrf2/HO-1 pathway.关键词
牡荆素/鼻咽癌/铁死亡/Nrf2/HO-1通路Key words
Vitexin/Nasopharyngeal carcinoma/Ferroptosis/Nrf2/HO-1 pathway引用本文复制引用
李艳峰,袁东杰,李靖,卢振民,王慧敏..基于Nrf2/HO-1通路介导的细胞铁死亡探究牡荆素对鼻咽癌细胞的作用机制研究[J].中医药信息,2025,42(9):27-35,9.基金项目
河南省高等学校重点科研项目(23B320122) （23B320122）
