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作 者:赵培彰 杨桢[2] 陈香云 陶旭光[3] 亓玉婕 何湛湛 褚策 袁雨露 丁薇 张雨欣 许咏琪 赵红霞[3] 汪文来[3] ZHAO Peizhang;YANG Zhen;CHEN Xiangyun;TAO Xuguang;QI Yujie;HE Zhanzhan;CHU Ce;YUAN Yulu;DING Wei;ZHANG Yuxin;XU Yongqi;ZHAO Hongxia;WANG Wenlai(West China Clinical Medical College,Sichuan University,Chengdu 610041,China;Beijing University of Chinese Medicine,Beijing 100029,China;Institute of Basic Theory for Traditional Chinese Medicine,China Academy of Chinese Medical Sciences,Beijing 100700,China)
机构地区:[1]四川大学华西临床医学院,成都610041 [2]北京中医药大学,北京100029 [3]中国中医科学院中医基础理论研究所,北京100700
出 处:《中国实验方剂学杂志》2023年第20期247-256,共10页Chinese Journal of Experimental Traditional Medical Formulae
基 金:中国中医科学院科技创新工程项目(CI2021A00606);中国中医科学院自主选题项目(YZX202237,YZ2020042);北京市中医药科技发展基金项目(JJ2018-99)。
摘 要:动脉粥样硬化(AS)是一种脂质堆积、血管内皮功能障碍导致的慢性炎症性疾病,Toll样受体(TLR)/核转录因子-κB(NF-κB)通路与NOD样受体蛋白3(NLRP3)炎性小体通路在动脉粥样硬化的产生中发挥着重要的致炎作用,而瞬时受体电位香草酸亚型1(TRPV1)与瞬时受体电位锚蛋白1(TRPA1)在动脉粥样硬化的发生过程中发挥着重要的保护作用。作者对近10年国内外期刊发表的相关研究进行梳理,研究显示,TRPV1/TRPA1的激活可以通过多种途径激活内皮型一氧化氮合酶(eNOS)、抑制活性氧(ROS)、抑制胆固醇晶体(CC)的产生进而调控TLR/NF-κB与NLRP3炎性小体通路,抑制TLR/NLRP3介导的炎症反应。同时,中医药中多种单味药有效成分与方剂可有效激活TRPV1/TRPA1或其下游途径,其对动脉粥样硬化中TLR/NLRP3通路可能具有显著调控作用。该文进一步对已探明的方剂及中药单味药有效成分调控AS中TLR/NLRP3通路的机制进行梳理,将TRPV1/TRPA1调控TLR/NLRP3途径的机制与中药方剂与单体成分进行对应。为治疗动脉粥样硬化的中药药物相互作用机制提供新启发,为临床中医药治疗动脉粥样硬化提供新策略。Atherosclerosis is a chronic inflammatory disease caused by lipid accumulation and vascular endothelial dysfunction.The Toll-like receptor(TLR)/nuclear transcription factor-κB(NF-κB)pathway and the NOD-like receptor protein 3(NLRP3)inflammasome pathway play a proinflammatory role,while the transient receptor potential vanilloid subtype 1(TRPV1)and transient receptor potential ankyrin 1(TRPA1)play a protective role in the occurrence of atherosclerosis.We reviewed the relevant studies published in the last 10 years.The results showed that activation of TRPV1/TRPA1 could activate endothelial-type nitric oxide synthase(eNOS)and inhibit the generation of reactive oxygen species(ROS)and cholesterol crystal(CC)to modulate the TLR/NF-κB and NLRP3 inflammasome pathways,thereby inhibiting TLR/NLRP3-mediated inflammatory response.A variety of compound prescriptions and active components of Chinese medicinal materials can activate TRPV1/TRPA1 or its downstream pathway to regulate the TLR/NLRP3 pathway in atherosclerosis.This paper introduces the mechanisms of compound prescriptions and active components of Chinese medicinal materials in regulating the TLR/NLRP3 pathway via TRPV1/TRPA1 in atherosclerosis.This review provides new ideas for the research on the interactions between Chinese medicines in the treatment of atherosclerosis and provides a new strategy for the clinical treatment of atherosclerosis with traditional Chinese medicine.
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