中国组织工程研究

中国组织工程研究 ›› 2025, Vol. 29 ›› Issue (34): 7431-7438.doi: 10.12307/2025.713

• 生物材料综述 biomaterial review • 上一篇    下一篇

抗氧化纳米药物介导心肌缺血再灌注损伤的靶向治疗

吴青芸1，2，苏  强1   

  1. 1广西壮族自治区江滨医院，广西壮族自治区南宁市  530021；2桂林医学院，广西壮族自治区桂林市  541004
  • 收稿日期:2024-09-02 接受日期:2024-10-16 出版日期:2025-12-08 发布日期:2025-01-17
  • 通讯作者: 苏强，博士，教授，广西壮族自治区江滨医院心血管内科，广西壮族自治区南宁市 530021
  • 作者简介:吴青芸，女，1997年生，贵州省凯里市人，苗族，在读硕士，主要从事心血管疾病的临床与基础研究。
  • 基金资助:
    国家自然科学基金项目(82260072)，项目负责人：苏强；广西自然科学基金重点项目(2020GXNSFDA238007)，项目负责人：苏强

Antioxidant nanomedicine-mediated targeted therapy for myocardial ischemia-reperfusion injury

Wu Qingyun1, 2, Su Qiang1   

  1. 1Jiangbin Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi Zhuang Autonomous Region, China; 2Guilin Medical University, Guilin 541004, Guangxi Zhuang Autonomous Region, China
  • Received:2024-09-02 Accepted:2024-10-16 Online:2025-12-08 Published:2025-01-17
  • Contact: Su Qiang, MD, Professor, Jiangbin Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi Zhuang Autonomous Region, China
  • About author:Wu Qingyun, Master’s degree, Jiangbin Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi Zhuang Autonomous Region, China; Guilin Medical University, Guilin 541004, Guangxi Zhuang Autonomous Region, China
  • Supported by:
    National Natural Science Foundation of China, No. 82260072 (to SQ); Key Natural Science Foundation Project of Guangxi, No. 2020GXNSFDA238007 (to SQ)

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摘要：


文题释义：

心肌缺血再灌注损伤：是指心肌缺血后血液和氧气再灌注对心肌细胞造成的损伤和炎症反应。心肌缺血再灌注损伤的严重程度取决于缺血持续时间、再灌注流速、氧含量和缺血区域的大小等因素。
氧化应激：是指体内氧化系统和抗氧化系统的失衡，导致有害活性氧(如超氧阴离子、羟自由基等)过量产生，进而引起细胞和组织损伤的一种状态。氧化应激与多种疾病的发生和发展密切相关，在心血管疾病方面与心肌缺血再灌注损伤关系密切。


背景：心肌缺血再灌注时过量活性氧会加速心肌损伤，抗氧化疗法虽有效但存在低生物利用度和靶向特异性差等局限性。纳米药物以精准靶向与延长药效的优势在心肌保护中展现出广阔应用前景。

目的：总结心肌再灌注损伤过程中活性氧产生的途径以及纳米医学治疗心肌缺血性损伤的最新进展。
方法：检索中国知网和PubMed数据库中关于抗氧化纳米药物介导心肌缺血再灌注损伤靶向治疗的相关文献，以“纳米，纳米药物，纳米材料，纳米技术，心肌缺血再灌注损伤，氧化应激，活性氧”为中文检索词，以“nanostructures，nanomedicine，nanomaterials，nanotechnology，myocardial ischemia reperfusion injury，oxidative stress，reactive oxygen species”为英文检索词，检索时限为2019年8月至2024年8月，通过阅读文献题目和摘要进行初步筛选，然后剔除与文章主题相关性不高的文献，最终纳入65篇文献进行分析。

结果与结论：高浓度活性氧的累积是心肌缺血再灌注损伤的核心机制之一。不同来源途径的活性氧能够直接干预物质与能量的代谢过程，进而触发心肌细胞的凋亡或坏死，对心脏组织构成显著损害，因此，清除或降低活性氧水平被视为有效遏制心肌缺血再灌注损伤发展的重要治疗策略。传统药物半衰期短、生物利用度低、缺乏靶向性，再加上肝脏和脾脏的螯合作用以及心肌部位血流的持续冲刷，严重影响了临床药物的预期疗效。纳米药物在突破上述局限方面展现出非凡的潜力，为缺血性疾病的治疗开辟了新方向。通过精确设计的纳米颗粒可实现对药物的靶向递送，显著提高药物在受损心肌部位的浓度与滞留时间，从而增强治疗效果。此外，纳米药物作为抗氧化剂、生长因子或细胞疗法的载体有效减轻了氧化应激，促进了心肌细胞的修复与再生，为心肌功能的恢复带来了希望。

https://orcid.org/0009-0003-4400-5049(吴青芸)

中国组织工程研究杂志出版内容重点：生物材料；骨生物材料；口腔生物材料；纳米材料；缓释材料；材料相容性；组织工程

关键词: 抗氧化, 纳米药物, 传统药物, 心肌缺血再灌注损伤, 急性心肌梗死, 氧化应激, 活性氧, 靶向治疗, 工程化血管材料

Abstract: BACKGROUND: Excessive reactive oxygen species accelerate myocardial injury during myocardial ischemia and reperfusion. Antioxidant therapies are effective but have limitations such as low bioavailability and poor target specificity. Nanomedicines, with their advantages of precise targeting and prolonged efficacy, show a broad application prospect in myocardial protection.
OBJECTIVE: To summarize the pathways of reactive oxygen species production during myocardial ischemia and the latest advances in nanomedicine for the treatment of myocardial ischemic injury.
METHODS: We searched CNKI and PubMed databases for relevant literature on antioxidant nanomedicine-mediated targeted therapy for myocardial ischemia- reperfusion injury, using “nano, nanomedicine, nanomaterials, nanotechnology, myocardial ischemia reperfusion injury, oxidative stress, reactive oxygen species” as Chinese search terms and “nanostructures, nanomedicine, nanomaterials, nanotechnology, myocardial ischemia reperfusion injury, oxidative stress, reactive oxygen species” as English search terms. The search time limit was from August 2019 to August 2024. Totally 65 articles were included in the analysis by reading the titles and abstracts of the literature for preliminary screening and excluding those with low relevance to the title of the literature.
RESULTS AND CONCLUSION: The buildup of high levels of reactive oxygen species is a key factor in myocardial ischemia-reperfusion injury. These reactive oxygen species, generated from various sources, can disrupt the metabolic processes of substances and energy, ultimately leading to apoptosis or necrosis of cardiomyocytes and causing significant damage to cardiac tissue. As a result, removing or reducing reactive oxygen species has become an important therapeutic approach to effectively prevent myocardial ischemia-reperfusion injury. Traditional medications often have short half-lives, low bioavailability, and lack targeted delivery. Additionally, the chelation effects of the liver and spleen, along with the continuous blood flow in the myocardial region, significantly impair the expected efficacy of these clinical drugs. Nanomedicines present a promising solution to these challenges and have opened new avenues for treating ischemic diseases. Carefully designed nanoparticles can facilitate targeted drug delivery, greatly increasing the concentration and retention of drugs in damaged myocardial areas, thereby enhancing therapeutic outcomes. Moreover, as carriers of antioxidants, growth factors, or cell therapies, nanomedicines effectively reduce oxidative stress and promote the repair and regeneration of cardiomyocytes, offering hope for restoring myocardial function. 

Key words: antioxidant, nanomedicine, conventional drug, myocardial ischemia-reperfusion injury, acute myocardial infarction, oxidative stress, reactive oxygen species, targeted therapy, engineered vascular material

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