Pharmacological Effects and Mechanisms of Chinese Medicines Modulating NLRP3 Inflammasomes in Ischemic Cardio/Cerebral Vascular Disease

炎症体 医学 中医药 药理学 白藜芦醇 自噬 机制(生物学) 程序性细胞死亡 传统医学 炎症 细胞凋亡 免疫学 生物 生物化学 病理 认识论 哲学 替代医学
作者
Yueying Li,Yuntao Liu,Yan Xia,Qing Liu,Yonghua Zhao,Dawei Wang
出处
期刊:The American Journal of Chinese Medicine [World Scientific]
卷期号:46 (08): 1727-1741 被引量:28
标识
DOI:10.1142/s0192415x18500878
摘要

Cardio/cerebral-vascular diseases seriously threaten human health and are the leading cause of death. As such, there is great interest in identifying a potential mechanism that controls the development process of cardio/cerebral vascular diseases. Present studies demonstrate that inflammasomes play an important role in the process of ischemic cardio/cerebral vascular diseases (ICCVDs). Among the pathological process of ICCVDs, inflammasomes activated the sterile inflammatory response that accelerated the development of diseases and aggravated the acute lesion of tissue. As the most thoroughly studied inflammasome, the NLRP3 inflammasome has been proven to be a potential therapeutic target for ICCVDs. In this review, we summarized the mechanisms of Chinese herbal medicine which can affect ICCVDs via the regulation of the NLRP3 inflammasome. Our study discovers that active compounds of Chinese medicines have a negative effect on NLRP3 in different ICCVDs models. Astragaloside IV may influence the receptor of the cell membrane to inhibit NLRP3 activation. Resveratrol, colchicinesis, salvianolic acid B, chrysophanol and sulforaphane may directly damage the formation of NLRP3 by inhibiting ASC or Caspase-1. Most of the active natural compounds can negatively regulate the downstream products of NLRP3 inflammasome such as IL-18 and IL1[Formula: see text]. In addition, Chinese medicines such as sinomenine, ruscogenin, resveratrol, arctigenin and cepharanthineas may downregulate NLRP3 inflammasome by inducing autophagy activation. Due to the advantages of multi-target effects, Chinese herbal medicine can be treated as a splendid therapy for ICCVDs by inhibiting NLRP3 inflammasome.
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