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首页|期刊导航|时珍国医国药|抗纤益心方通过MCU通路改善扩张型心肌病小鼠心肌纤维化的研究

抗纤益心方通过MCU通路改善扩张型心肌病小鼠心肌纤维化的研究

何平鸽 薛祎琨 常红波 王素云 孔桂选 赵文静 李骋 王少昂 王振涛

时珍国医国药2026,Vol.37Issue(5):829-835,7.
时珍国医国药2026,Vol.37Issue(5):829-835,7.DOI:10.70976/j.1008-0805.SZGYGY-2026-0505

抗纤益心方通过MCU通路改善扩张型心肌病小鼠心肌纤维化的研究

Study on the improvement of myocardial fibrosis in mice with dilated cardiomyopathy by Kangxian Yixin Formula(抗纤益心方)via the MCU pathway

何平鸽 1薛祎琨 1常红波 1王素云 1孔桂选 1赵文静 1李骋 1王少昂 1王振涛2

作者信息

  • 1. 河南中医药大学第二临床医学院,河南 郑州 450053
  • 2. 河南中医药大学第二临床医学院,河南 郑州 450053||河南省中医院,河南 郑州 450053
  • 折叠

摘要

Abstract

Objective To investigate the effect of Kangxian Yixin Formula(抗纤益心方,KXYXF)on myocardial fibrosis(MF)in mice with dilated cardiomyopathy(DCM)and its relationship with the mitochondrial calcium uniporter(MCU)-mediated calcium signal-ing pathway.Methods Forty DCM model mice were randomly divided into four groups(n=10 per group):model,KXYXF,captopril,and KXYXF+captopril combination.An additional 10 healthy mice served as the normal control group.After 8 weeks of treatment,car-diac function was evaluated by echocardiography,measuring left ventricular end-diastolic diameter(LVEDd),left ventricular ejection fraction(LVEF),and left ventricular fractional shortening(LVFS).Myocardial pathology and collagen deposition were assessed by hematoxylin-eosin(HE)and Masson staining.Mitochondrial ultrastructure was examined by transmission electron microscopy(TEM).The expression of MCU,calmodulin(CaM),nuclear factor of activated T cells 4(NFAT4),collagen type I(COL-1),and alpha-smooth muscle actin(α-SMA)was detected at the mRNA and protein levels by polymerase chain reaction(PCR)and Western blot(WB),respectively.Results Compared with the normal control group,the model group exhibited impaired cardiac function(increased LVEDd,decreased LVEF and LVFS),disorganized myocardial architecture,significant fibrosis,mitochondrial damage,and upregu-lated expression of MCU,CaM,NFAT4,COL-1,and α-SMA(P<0.05 or P<0.01).Treatment with KXYXF significantly improved cardiac function,attenuated MF and mitochondrial injury,and downregulated the expression of MCU,CaM,NFAT4,α-SMA,and COL-1 compared with the model group(P<0.05 or P<0.01).Conclusion KXYXF alleviates MF and improves cardiac function in DCM mice,potentially through modulation of the MCU-mediated calcium transport pathway.

关键词

抗纤益心方/扩张型心肌病/心肌纤维化/线粒体钙单向转运体

Key words

Kangxian Yixin Formula(抗纤益心方)/Dilated cardiomyopathy/Myocardial fibrosis/Mitochondrial calcium uni-porter

分类

医药卫生

引用本文复制引用

何平鸽,薛祎琨,常红波,王素云,孔桂选,赵文静,李骋,王少昂,王振涛..抗纤益心方通过MCU通路改善扩张型心肌病小鼠心肌纤维化的研究[J].时珍国医国药,2026,37(5):829-835,7.

基金项目

国家自然科学基金青年基金资助项目(82205082) (82205082)

河南省重点研发与推广专项(科技攻关(222102310482) (科技攻关(222102310482)

河南省中医药科学研究专项(2021JDZX2103) (2021JDZX2103)

时珍国医国药

1008-0805

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