[关键词]
[摘要]
急性心肌梗死以高死亡率、预后极差等特点严重威胁人类生命健康,常以经皮冠状动脉介入术恢复血供,治疗的同时易出现心肌缺血再灌注损伤(MIRI)等严重并发症。目前,临床上关于MIRI发生机制及治疗方法仍存在空缺,因此,积极探寻减轻MIRI的方法对维护人类生命安全有重大意义。中药的有效成分在MIRI治疗方面有显著疗效,其中生物碱类中药单体可通过调控多种通路减轻MIRI,如吗啡激活丝裂原活化蛋白激酶(MAPK)信号通路、胡椒碱激活磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)信号通路、苦参碱激活缺氧诱导因子-1α(HIF-1α)信号通路、异莲心碱激活核因子E2相关因子2/血红素加氧酶1(Nrf2/HO-1)信号通路、α-玉柏碱抑制基质金属蛋白酶(MMP)信号通路等,以达到抑制细胞凋亡、细胞自噬、氧化应激、炎症反应、线粒体损伤等作用。对生物碱类中药单体作用于多种信号通路治疗MIRI的相关机制进行综述,为减缓MIRI的发生发展提供理论基础。
[Key word]
[Abstract]
Acute myocardial infarction is a serious threat to human life and health due to its high mortality and poor prognosis. Percutaneous coronary intervention is often used to restore blood supply. At the same time, it is prone to serious complications such as myocardial ischemia-reperfusion injury (MIRI). At present, the clinical mechanism and treatment of MIRI are still vacant. Therefore, it is of great significance to actively explore ways to reduce MIRI to maintain human life safety. The effective components of traditional Chinese medicine have a significant effect in the treatment of MIRI, and alkaloids can reduce MIRI by regulating multiple pathways, such as morphine activates mitogen-activated protein kinase (MAPK) signaling pathway, piperine activates phosphatidylinositol 3 kinase/kinase B (PI3K/Akt) signaling pathway, matrine activates hypoxia inducible factor-1α (HIF-1α) signaling pathway, isoliensinine activates nuclear factor erythroid 2 related factor 2/heme oxygenase 1 (Nrf2/HO-1) signaling pathway,α-obscurine inhibition matrix metalloproteinase (MMP) signaling pathway, etc. In order to inhibit apoptosis, autophagy, oxidative stress, inflammatory response, mitochondrial damage and so on. This article reviews the relevant mechanisms of alkaloid based traditional Chinese medicine monomers acting on multiple signaling pathways, and provides a theoretical basis for slowing down the occurrence and development of MIRI.
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[基金项目]
国家教育部产学合作协同育人项目(220904439201225);国家级大学生创新创业训练计划项目(S202312661006);湖南中医药大学教学改革研究项目(2023-JG011);湖南中医药大学-湖南中和大汉健康产业运营管理有限公司联合基金项目(02);湖南中医药大学本科生科研创新基金项目资助(2023BKS015)