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<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">MRP</journal-id><journal-title-group><journal-title>Medical Research and Practice</journal-title></journal-title-group><issn>2993-9690</issn><eissn>2993-9704</eissn><publisher><publisher-name>Art and Technology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.61369/MRP.2026050009</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>龙血素A 对JAK2/STAT3信号通路减轻MIRI的机制研究</title><url>https://artdesignp.com/journal/MRP/4/5/10.61369/MRP.2026050009</url><author>魏成磊,黄照河</author><pub-date pub-type="publication-year"><year>2026</year></pub-date><volume>4</volume><issue>5</issue><history><date date-type="pub"><published-time>2026-05-20</published-time></date></history><abstract>心血管疾病已成为严重威胁人类健康的重大公共卫生问题，心肌梗死致死率居高不下。临床血运重建虽能挽救缺血心肌，但可引发心肌缺血再灌注损伤（MIRI），其机制与活性氧大量生成、细胞凋亡异常及炎症反应密切相关，最终可导致心功能下降甚至心力衰竭。目前MIRI的临床干预效果有限，机制尚未完全阐明，亟需探索新的治疗靶点。JAK2/STAT3信号通路在MIRI中具有重要心肌保护作用，可通过抑制氧化应激、凋亡与炎症发挥心脏保护效应。研究表明，龙血素能够调控该通路减轻心肌损伤，而龙血素A作为龙血竭的主要活性成分，其通过JAK2/STAT3通路干预MIRI 的具体机制仍有待系统阐明。本文就相关研究进行综述，旨在为心肌缺血再灌注损伤的防治提供理论依据，推动中医药在心血管疾病中的应用与发展。</abstract><keywords>心肌缺血再灌注损伤,JAK2/STAT3信号通路,龙血素A</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[1] 刘明波, 何新叶, 杨晓红, 等.《中国心血管健康与疾病报告2024》要点解读[J].中国全科医学,2025,28(32):3989-4008..[2]Algoet M, Janssens S, Himmelreich U, et al. Myocardial ischemia-reperfusion injury and the influence of inflammation[J]. Trends in Cardiovascular Medicine,2023,33(6):357-366.DOI:10.1016/j.tcm.2022.02.005.[3]Mahdiani S, Omidkhoda N, Rezaee R, et al. Induction of JAK2/STAT3 pathway contributes to protective effects of different therapeutics against myocardial ischemia/reperfusion[J]. Biomed Pharmacother, 2022,155:113751.DOI:10.1016/j.biopha.2022.113751.
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