中药调控NLRP3炎症小体改善心肌纤维化的研究进展
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篇名: 中药调控NLRP3炎症小体改善心肌纤维化的研究进展
TITLE: Research progress on the improvement of myocardial fibrosis by traditional Chinese medicine through regulation of NLRP3 inflammasome
摘要: 心肌纤维化(MF)以心功能和心肌顺应性下降为特征,是多种心血管疾病的共同病理过程及进展因素。核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体3(NLRP3)炎症小体与MF发生发展密切相关。近年有研究表明,中药可通过调控NLRP3炎症小体来缓解MF。基于此,本文通过系统总结中药调控NLRP3炎症小体改善MF的作用机制研究进展,发现生物碱类(石蒜碱、长春新碱、蟾蜍灵)、皂苷类(黄芪甲苷、薯蓣皂苷、人参皂苷Rg3)、萜类(雷公藤红素、冬凌草甲素)、酚类(白藜芦醇苷、姜黄素、根皮苷)等中药单体及复方(扎冲十三味丸、蛭龙活血通瘀胶囊、鹿芪方)可通过抑制NLRP3炎症小体活化,进而抑制炎症因子如白细胞介素1β(IL-1β)和IL-18释放,减轻心肌组织炎症反应损伤,减少细胞外基质过度沉积,从而发挥改善MF的作用。
ABSTRACT: Myocardial fibrosis (MF), characterized by decreased cardiac function and myocardial compliance, is a pathological process and a progression factor in various cardiovascular diseases. The nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) inflammasome is closely related to the development of MF. Recent studies have shown that traditional Chinese medicine (TCM) can regulate the NLRP3 inflammasome to alleviate MF. Based on this, this article systematically summarizes the research progress on the mechanisms by which TCM regulates the NLRP3 inflammasome to improve MF. It is found that active ingredients of TCM, such as alkaloids (lycorine,vincristine,bufalin), saponins (astragaloside Ⅳ, diosgenin,ginsenoside Rg3), terpenoids (celastrol,oridonin), and phenols (polydatin,curcumin,phloridzin) as well as TCM formulas (Zhachong shisanwei pills,Zhilong huoxue tongyu capsules, Luqi formula) can inhibit the activation of the NLRP3 inflammasome, thereby suppressing the release of inflammatory factors such as interleukin-1β and IL-18, reducing inflammatory damage to myocardial tissue, alleviating excessive deposition of the extracellular matrix, and thus exerting the effect of improving MF.
期刊: 2025年第36卷第08期
作者: 张瑞;闫景顺;贾福运;贾轲欣;刘晨阳;刘岩;李烨;徐强
AUTHORS: ZHANG Rui,YAN Jingshun,JIA Fuyun,JIA Kexin,LIU Chenyang,LIU Yan,LI Ye,XU Qiang
关键字: 中药单体;中药复方;心肌纤维化;NLRP3炎症小体;作用机制
KEYWORDS: active component of TCM; TCM formula; myocardial fibrosis; NLRP3 inflammasome; mechanism of action
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