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铁代谢与缺血性脑卒中 被引量:9

Relationship between iron metabolism and ischemic stroke
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摘要 背景:缺血性脑卒中是临床上的主要致死及致残性疾病,目前尚无有效的解决方案。铁代谢异常与多种生理和病理生理过程有关,最新发现其与缺血性脑卒中密切相关。目的:探讨铁代谢与缺血性脑卒中的关系,以新颖的视角寻找缺血性脑卒中的潜在新治疗靶点,以期指导缺血性脑卒中的治疗。方法:以“iron metabolism,ischemic stroke,reactive oxygen species,glutathione peroxidase 4,blood-brain barrier,inflammatory factors,excitatory amino acid,Tau,oligodendrocytes,autophagy,iron death,serum ferritin”为英文检索词,以“铁代谢,缺血性脑卒中,活性氧自由基,谷胱甘肽过氧化物酶4,血脑屏障,炎症因子,兴奋性氨基酸,Tau蛋白,少突胶质细胞,自噬,铁死亡,血清铁蛋白”为中文检索词,应用计算机检索2010年1月至2022年1月PubMed、CNKI及万方数据库收录的相关文献,最终纳入文献82篇进行归纳分析。结果与结论:①铁代谢平衡对维持大脑神经元的正常生命活动是至关重要的,脑缺血后铁代谢失衡可参与多种病理生理过程,进一步加重脑缺血后继发性脑损伤;②以铁代谢为靶点治疗缺血性脑卒中可有效减轻脑缺血后继发性脑损伤,促进神经功能恢复;③目前缺血性脑卒中后继发性脑损伤与铁之间关系的研究相对较少,其详实的病理生理机制仍未阐明,相关治疗策略也需进一步完善,因此更需要深入研究铁代谢在缺血性脑卒中后的作用机制,可为缺血性脑卒中后继发性脑损伤的治疗提供新的干预靶点。 BACKGROUND:Ischemic stroke is a major clinically fatal and disabling disease and there is no effective solution yet.Abnormal iron metabolism is related to various physiological and pathophysiological processes,and the latest discovery is that it is closely related to ischemic stroke.OBJECTIVE:To explo re the relationship between iron metabolism and ischemic stroke and look for potential new therapeutic targets for ischemic stroke from a novel perspective,in order to guide the treatment of ischemic stroke.METHODS:We searched for relevant literature from January 2010 to January 2022 in PubMed,CNKI,and WanFang databases.The search terms were "iron metabolism,ischemic stroke,reactive oxygen species,glutathione peroxidase 4,blood-brain barrier,inflammatory factors,excitatory amino acid,Tau,oligodendrocytes,autophagy,iron death,serum ferritin" in English and Chinese.Finally,82 articles were included for further analysis.RESULTS AND CONCLUSION:(1) The balance of iron metabolism is essential to maintain the normal life activities of brain neurons.Iron metabolism imbalance can participate in a variety of pathophysiological processes to further aggravate secondary brain injury after cerebral ischemia.(2) Treatments of ischemic stroke with iron metabolism as a target can effectively reduce secondary brain injury after cerebral ischemia and promote nerve function recovery.(3) At present,there are relatively few studies on the relationship between secondary brain injury and iron after ischemic stroke.The detailed pathophysiological mechanism has not yet been elu cidated,and related treatment strategies need to be further improved.Therefore,it is necessary to further study the mechanism of iron metabolism after ischemic stro ke,which may provide a new target for the treatment of secondary brain injury after ischemic stroke.
作者 凡勇福 苏凯奇 袁洁 聂晨晨 阮晓迪 段昭远 冯晓东 Fan Yongfu;Su Kaiqi;Yuan Jie;Nie Chenchen;Ruan Xiaodi;Duan Zhaoyuan;Feng Xiaodong(Henan University of Chinese Medicine,Zhengzhou 450000,Henan Province,China;Rehabilitation Center,the First Affiliated Hospital of Henan University of Chinese Medicine,Zhengzhou 450000,Henan Province,China)
出处 《中国组织工程研究》 CAS 北大核心 2022年第32期5223-5228,共6页 Chinese Journal of Tissue Engineering Research
基金 国家自然科学基金面上项目(82174473),项目负责人:冯晓东 国家自然科学联合基金项目(U2004131),项目负责人:冯晓东 河南省中医药科学研究专项课题(2018JDZX011),项目负责人:冯晓东 河南省科技攻关计划(202102310167) 项目负责人:冯晓东。
关键词 缺血性脑卒中 铁代谢 继发性脑损伤 活性氧自由基 铁死亡 ischemic stroke iron metabolism secondary brain injury reactive oxygen species iron death
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  • 1FloydRA. Role of oxygen free radicals in carcinogenesis and brain ischemia. FASEB J, 1990, 4(9):2587-2597.
  • 2AscherioA, WillettWC. Are body iron stores related to the risk of coronary heart disease?. N Engl J Med, 1994, 330(16):1152-1154. DOI: 10.1056/NEJM199404213301611.
  • 3PraticóD, PasinM, BarryOP, et al. Iron-dependent human platelet activation and hydroxyl radical formation: involvement of protein kinase C. Circulation, 1999, 99(24):3118-3124. DOI: 10.1161/01.CIR.99.24.3118.
  • 4KondoY, OgawaN, AsanumaM, et al. Regional differences in late-onset iron deposition, ferritin, transferrin, astrocyte proliferation, and microglial activation after transient forebrain ischemia in rat brain. J Cereb Blood Flow Metab, 1995, 15(2):216-226. DOI: 10.1038/jcbfm.1995.27.
  • 5PalmerC, MenziesSL, RobertsRL, et al. Changes in iron histochemistry after hypoxic-ischemic brain injury in the neonatal rat. J Neurosci Res, 1999, 56(1):60-71. DOI: 10.1002/(SICI)1097-4547(19990401)56:13.3.CO;2-1.
  • 6PalmerC, RobertsRL, BeroC. Deferoxamine posttreatment reduces ischemic brain injury in neonatal rats. Stroke, 1994, 25(5):1039-1045. DOI: 10.1161/01.STR.25.5.1039.
  • 7FengY, LeBlancMH, LeBlancEB, et al. Desmethyl tirilazad improves neurologic function after hypoxic ischemic brain injury in piglets. Crit Care Med, 2000, 28(5):1431-1438. DOI: 10.1097/00003246-200005000-00029.
  • 8DávalosA, CastilloJ, MarrugatJ, et al. Body iron stores and early neurologic deterioration in acute cerebral infarction. Neurology, 2000, 54(8):1568-1574. DOI: 10.1212/WNL.54.8.1568.
  • 9PantoniL. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. Lancet Neurol, 2010, 9(7):689-701. DOI: 10.1016/S1474-4422(10)70104-6.
  • 10HaackeEM, ChengNY, HouseMJ, et al. Imaging iron stores in the brain using magnetic resonance imaging. Magn Reson Imaging, 2005, 23(1):1-25. DOI: 10.1016/j.mri.2004.10.001.

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