期刊文献+

PPARα的生物学特征及其在脑梗死中作用的研究进展 被引量:2

Research progress on the biological characteristics of PPARα and its role in cerebral infarction
下载PDF
导出
摘要 过氧化物酶体增殖物激活受体α(peroxisome proliferators-activatedreceptorα,PPARα)为一类配体依赖的转录调节因子,被其配体或激动剂激活后在众多病理生理过程中具有重要作用。PPARα在脑组织的不同部位和神经细胞中均有表达,参与调节脑梗死后炎症反应、氧化应激、细胞凋亡、血脑屏障功能等多种病理生理过程,从而发挥减轻缺血性脑损伤的作用。除此之外,PPARα能通过控制肥胖、改善胰岛素抵抗和降低血脂等途径减少脑梗死发病率。因此,PPARα可能成为预防脑梗死发生和治疗脑梗死的新靶标。本文针对PPARα的生物学特征及其在脑梗死中作用的研究进展进行综述。 Peroxisome proliferation-activated receptor α(PPARα) is one of the ligand-dependent transcriptional regulatory factors that play important roles in a variety of pathophysiological processes when they are activated by their ligands or agonists. PPARα is expressed in different parts of brain tissue and nerve cells, involving in the regulation of various pathophysiological processes such as inflammation, oxidative stress, apoptosis, and blood-brain barrier function after cerebral infarction, hence plays a role in treating ischemic brain injury. In addition, PPARα can reduce the incidence of cerebral infarction by controlling obesity, improving insulin resistance and lowering blood lipids. Therefore, PPARα may become a new target for the prevention and treatment of cerebral infarction. This article reviews the research progress of the biological characteristics of PPARα and its role in cerebral infarction.
作者 官劲帆 韩江全 安露露 田明巧 GUAN Jinfan;HAN Jiangquan;AN Lulu;TIAN Mingqiao(Department of Neurology,the Fifth Affiliated Hospital of Zunyi Medical University,Zhuhai 519100,China)
出处 《大连医科大学学报》 CAS 2021年第6期554-560,共7页 Journal of Dalian Medical University
基金 “十四五”期间珠海市临床重点专科建设项目(珠卫函[2021]115号) 遵义市科技计划资助项目(遵市科合社字[2018]20号)。
关键词 脑梗死 过氧化物酶体增殖物激活受体Α 病理过程 危险因素 ischemic stroke PPARα pathological process risk factors
  • 相关文献

参考文献5

二级参考文献115

  • 1各类脑血管疾病诊断要点[J].中华神经科杂志,1996,29(6):379-380. 被引量:33037
  • 2Murphy MP.How mitochondria produce reactive oxygen speciesBiochemical Journal,2009.
  • 3Neve BP;Corseaux D;Chinetti G.PPARalpha agonists inhibit tissue factor expression in human monocytes and macrophages,2001.
  • 4Nissen SE;Wolski K.Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes,2007(24).
  • 5Sawyer DB;Siwik DA;Xiao L;Pimentel DR Singh K Colucci WS.Role of oxidative stress in myocardial hypertrophy and failure,2002(04).
  • 6Klewer S A,Xu H E,Lambert M H,et al.Peroxisome proliferator-activated receptors: from genes to physiology. Recent Progress in Hormone Research . 2001
  • 7Staels B,Koenig W,Habib A,Merval R,Lebret M,Torra IP,Delerive P,Fadel A,Chinetti G,Fruchart JC,Najib J,Maclouf J,Tedgui A.Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators. Nature . 1998
  • 8Yue Tl TL,Chen J,Bao W,Narayanan PK,Bril A,Jiang W,Lysko PG,Gu JL,Boyce R,Zimmerman DM,Hart TK,Buck-ingham RE,Ohlstein EH.In vivo myocardial protection from ischemia/reperfusion injury by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone. Circulation . 2001
  • 9Asakawa M,Takano H,Nagai T,et al.Peroxisome proliferator-activated receptorγ plays a critical role in inhibition of cardiac hypertrophy in vitro and in vivo. Circulation . 2002
  • 10Khandoudi N,Delerive P,Berrebi-Bertrand I,et al.Rosiglitazone, a peroxisome proliferator-activated receptor-gamma, inhibits the Jun NH(2)-terminal kinase/activating protein 1 pathway and protects the heart from ischemia/ reperfusion injury. Diabetes . 2002

共引文献59

同被引文献28

引证文献2

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部