中国药房2026，Vol.37Issue(15)：1966-1973,8.DOI:10.6039/j.issn.1001-0408.2026.15.06
强心汤调控IκBα/NF-κB p65信号通路介导的巨噬细胞M1极化治疗慢性心力衰竭的作用机制
Mechanism of action of Qiangxin decoction in regulating the IκBα/NF-κB p65 signaling pathway-mediated M1 macrophage polarization for the treatment of chronic heart failure
摘要
Abstract
OBJECTIVE To explore the mechanism of Qiangxin decoction in the treatment of chronic heart failure(CHF)by regulating the inhibitor of nuclear factor-κB alpha/nuclear factor-κB p65 subunit(IκBα/NF-κB p65)signaling pathway-mediated M1 macrophage polarization.METHODS In animal experiments,mice were used as research subjects,and the CHF model was established via coronary artery ligation.Model mice were treated with Qiangxin decoction(21.69 g/kg)for 28 days.After intervention,pathological morphological changes of myocardial tissues and cardiomyocyte apoptosis were observed.Serum levels of inflammatory factors including tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6),myocardial injury marker troponin I3(TNNI3),and macrophage-related markers F4/80 and cluster of differentiation 80(CD80)were detected.In cell experiments,monocyte-macrophage leukemia RAW264.7 cells were induced to undergo M1 polarization by 10 ng/mL lipopolysaccharide combined with 10 ng/mL interferon-γ,followed by 48 h intervention with 10%drug-containing serum of Qiangxin decoction.After intervention,the nuclear translocation of NF-κB p65 and NF-κB p50 was observed.The positive rate of CD80 in cells was measured.The mRNA expression of inflammatory factors including IL-1β,IL-6,IL-8,IL-18,TNF-α,inducible nitric oxide synthase(iNOS),cyclooxygenase-2(COX2),C-C motif chemokine receptor 7 isoform 2(CCR7-2),as well as the expression levels of proteins related to the IκBα/NF-κB p65 signaling pathway were detected.RESULTS Animal experimental results showed that Qiangxin decoction alleviated myocardial fibrosis in mice,and significantly reduced the cardiomyocyte apoptosis rate,serum levels of TNF-α and IL-6,as well as the protein expression of TNNI3,F4/80 and CD80 in myocardial tissues(P＜0.05).Cell experimental results indicated that Qiangxin decoction significantly suppressed the nuclear translocation of NF-κB p65 and NF-κB p50(P＜0.05).It significantly decreased the CD80 positive rate,mRNA levels of IL-1β,IL-6,IL-8,IL-18,TNF-α,iNOS,COX2 and CCR7-2,total and nuclear expression of NF-κB p65,total,nuclear and cytoplasmic expression of phosphorylated NF-κB p65,total expression of phosphorylated IκBα(P＜0.05).Meanwhile,it significantly elevated the total expression of IκBα and cytoplasmic expression of NF-κB p65(P＜0.05).CONCLUSIONS Qiangxin decoction can inhibit the activity of the IκBα/NF-κB p65 signaling pathway,reduce the release of pro-inflammatory factors,thereby restraining M1 macrophage polarization,mitigating myocardial fibrosis,and ultimately exerting therapeutic effects against CHF.关键词
强心汤/慢性心力衰竭/IκBα/NF-κB p65信号通路/巨噬细胞M1极化/炎症反应Key words
Qiangxin decoction/chronic heart failure/IκBα/NF-κB p65 signaling pathway/M1 macrophage polarization/inflammatory response分类
医药卫生引用本文复制引用
石炜琦,卢健棋,朱智德,唐梅玲,肖湘,邹珊芸,涂雅柔,胡莉惠..强心汤调控IκBα/NF-κB p65信号通路介导的巨噬细胞M1极化治疗慢性心力衰竭的作用机制[J].中国药房,2026,37(15):1966-1973,8.基金项目
国家自然科学基金地区科学基金项目(No.82160887) （No.82160887）
广西中医药大学2025年校级博士研究生科研创新项目(No.YCBXJ2025016) （No.YCBXJ2025016）
