首页|期刊导航|医学分子生物学杂志|芪红胶囊对冠状动脉微血管疾病小鼠血管内皮细胞氧化应激的影响

芪红胶囊对冠状动脉微血管疾病小鼠血管内皮细胞氧化应激的影响OA

Effect of Qihong Capsules on Oxidative Stress in Vascular Endothelial Cells of Mice with Coronary Microvascular Disease

中文摘要英文摘要

目的 探讨芪红胶囊基于TLR4/NF-κB/GPX4 通路对冠状动脉微血管疾病(coronary microvascular disease,CMVD)小鼠线粒体氧化应激的影响.方法 将20 只CMVD模型小鼠随机分为模型组和芪红胶囊治疗组[0.648 g/(kg·d),灌胃4 周],另设10 只为对照组.通过HE、油红O染色及免疫组织化学评估冠状动脉病理和巨噬细胞浸润;采用蛋白质印迹和ELISA检测相关蛋白及活性氧(ROS)水平.结果 与对照组相比,模型组小鼠冠状动脉损伤严重,炎症因子(TNF-α、IL-1β、IL-6)表达及TLR4/NF-κB通路活化增强,GPX4、Sirt1、HO-1 表达降低,ROS升高(P<0.001).芪红胶囊干预后,上述病理改变显著改善,炎症与氧化应激受到抑制,保护性蛋白表达上调(P<0.001).结论 芪红胶囊可通过抑制TLR4/NF-κB炎症通路、上调GPX4/Sirt1/HO-1 表达,减轻氧化应激,从而改善CMVD小鼠微血管功能障碍,其机制可能与抑制铁死亡有关,体现多靶点干预潜力.

Objective To investigate the effect of Qihong capsules on mitochondrial oxidative stress in mice with coronary microvascular disease(CMVD)via the TLR4/NF-κB/GPX4 path-way.Methods Twenty CMVD model mice were randomly assigned to 2 groups:model group and Qihong capsules treatment group[0.648 g/(kg·d),intragastric administration for 4 weeks],and additional 10 mice were served as the control group.Hematoxylin-eosin(HE)staining,oil red O staining,and immunohistochemistry were employed to assess coronary pathology and macrophage infiltration.Western blotting and enzyme-linked immunosorbent assay(ELISA)were utilized to de-tect the expression of relevant proteins and levels of reactive oxygen species(ROS).Results Com-pared with the control group,the model group exhibited severe coronary artery injury,elevated ex-pression of inflammatory cytokines(TNF-α,IL-1β,IL-6),enhanced activation of the TLR4/NF-κB pathway,downregulated expression of GPX4,Sirt1,and HO-1,and increased ROS levels(all P<0.001).Following intervention with Qihong capsules,the aforementioned pathological changes were significantly ameliorated,inflammation and oxidative stress were suppressed,and the expression of protective proteins was upregulated(all P<0.001).Conclusion Qihong capsules can alleviate oxidative stress by inhibiting the TLR4/NF-κB inflammatory pathway and upregulating the expression of GPX4/Sirt1/HO-1,thereby improving microvascular dysfunction in CMVD mice.Its mechanism may be associated with the inhibition of ferroptosis,reflecting its potential for multi-target intervention.

高玉;王晓峰;姜海兵;吴竞辉;范辉

新疆医科大学第四临床医学院 乌鲁木齐市,830000新疆医科大学第四临床医学院 乌鲁木齐市,830000新疆医科大学第四临床医学院 乌鲁木齐市,830000天津中医药大学中医学院 天津市,301617新疆医科大学第四临床医学院 乌鲁木齐市,830000

医药卫生

冠状动脉微血管疾病芪红胶囊氧化应激TLR4/NF-κB/GPX4通路铁死亡

coronary microvascular diseaseQihong capsuleoxidative stressTLR4/NF-κB/GPX4 pathwayferroptosis

《医学分子生物学杂志》 2026 (2)

143-149,7

2023年度"天山英才"医药卫生人才培养计划项目(No.TSYC202301B053、No.TSYC202301B169) This work was supported by grants from the 2023"Tianshan Talent"Medical and Health Talent Training Program(No.TSYC202301B053,No.TSYC202301B169)

10.3870/j.issn.1672-8009.2026.02.005

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