中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (10): 4933-4944.doi: 10.4103/NRR.NRR-D-25-00399

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

远红外照射恢复线粒体动态改善缺血性脑卒中

  

  • 出版日期:2026-10-15 发布日期:2026-06-13

Far-infrared irradiation restores mitochondrial dynamics to ameliorate ischemic stroke

Wanyu Wu1, Yuping Wang1, 2, Bo Qin1, 2, Xiongfei Xu1, 3, Yuanqing Qu1, Nick Wang4, Wuyan Zheng1, Xiaoyun Yun1, Betty Yuen-Kwan Law1, Jianfeng Sun1, Wei Zhang1, Chang Chen1, 5, *, Vincent Kam-Wai Wong1, *   

  1. 1Dr. Neher’s Biophysics Laboratory for Innovative Drug Discovery, State Key Laboratory of Mechanism and Quality of Chinese Medicine, Faculty of Chinese Medicine, Macau University of Science and Technology, Macao Special Administrative Region, China; 
    2The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Southwest Medical University, Luzhou, Sichuan Province, China; 
    3The Affiliated Hospital of Southwest Medical University, Southwest Medical University, Luzhou, Sichuan Province, China; 
    4New Age Technology (Asia) Limited, Hong Kong Special Administrative Region, China; 
    5Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China
  • Online:2026-10-15 Published:2026-06-13
  • Contact: Vincent Kam-Wai Wong, PhD, kawwong@must.edu.mo; Chang Chen, MD, cchen@icmm.ac.cn.
  • Supported by:
    This work was supported by the FDCT grant from the Macao Science and Technology Development Fund, Nos. 0124/2022/A; 002/2023/ALC (to VKWW).

摘要:

缺血性脑卒中治疗手段仍受限于狭窄的治疗窗口期及副作用问题。远红外辐射在慢性疾病治疗中展现出潜力,但其在缺血性脑卒中中调节线粒体动态的作用尚不明确。实验采用大鼠大脑中动脉阻塞模型及氧糖剥夺损伤神经元细胞,探索远红外线的神经保护效应。每日30分钟远红外线照射可减少大脑中动脉阻塞大鼠模型梗死体积、减轻脑水肿并改善神经功能。蛋白质组学分析发现远红外线介导了包括线粒体融合调节蛋白视神经萎缩1在内的8种蛋白上调。在氧糖剥夺损伤细胞中,远红外辐射通过诱导视神经萎缩1表达恢复线粒体膜电位并增强融合。机制研究表明,远红外辐射通过提升视神经萎缩1表达稳定线粒体动态,从而减轻氧化应激并维持能量生成。敲低视神经萎缩1表达可部分抵消远红外辐射的保护效应。此研究确立了远红外辐射作为针对缺血性脑卒中中线粒体氧化还原稳态的非药物干预手段,为脑血管疾病治疗开辟了新途径。


https://orcid.org/0000-0002-2951-8108 (Vincent Kam-Wai Wong); https://orcid.org/0000-0003-1674-973X (Chang Chen)

关键词: 缺血性卒中, 远红外辐射, 线粒体动力学, 线粒体融合, 大脑中动脉阻塞, 神经保护, 氧化应激, 能量代谢

Abstract: Far-infrared irradiation exhibits promise in chronic diseases, and its role in ischemic stroke  specifically in modulating mitochondrial dynamics remains unknown. This study explored the neuroprotective effects of far-infrared irradiation using a rat middle cerebral artery occlusion model and oxygen-glucose deprivation-injured neuronal cells. In middle cerebral artery occlusion rats, daily 30-minute far-infrared irradiation treatment reduced infarct volume, alleviated cerebral edema, and improved neurological function. Proteomic analysis identified far-infrared irradiation-mediated upregulation of eight proteins, including the mitochondrial fusion regulator optic atrophy 1. In oxygen-glucose deprivation-exposed cells, far-infrared irradiation restored mitochondrial membrane potential, and enhanced fusion via optic atrophy 1 induction. Mechanistically, far-infrared irradiation stabilized mitochondrial dynamics by boosting optic atrophy 1 expression, thereby reducing oxidative stress and maintaining energy production. Optic atrophy 1 knockdown partly abolished the protective effects of far-infrared irradiation therapy. These results establish far-infrared irradiation as a non-pharmacological intervention targeting mitochondrial redox homeostasis in ischemic stroke, offering a novel therapeutic avenue for cerebrovascular disorders.

Key words: energy metabolism, far-infrared irradiation, ischemic stroke, middle cerebral artery occlusion (MCAO), mitochondrial dynamics, mitochondrial fusion, neuroprotection, optic atrophy 1 (Opa1), oxidative stress