缺血性脑卒中引发兴奋性氨基酸毒性激活RhoA通路抑制神经再生的机制研究  被引量:3

Study on the Mechanism of Inhibition of Nerve Regeneration by Activating Rhoa Signaling Pathway Induced by Excitatory Amino Acid Toxicity in Ischemic Stroke

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作  者:甘红霞 范有明 GAN Hongxia;FAN Youming(Hubei Minzu University Medical Center,Enshi 445000,Hubei,China;People's Hosptial of Chongqing Banan District of Changqing Medicine University,Chongqing 401320,China)

机构地区:[1]湖北民族大学医学部,湖北恩施445000 [2]重庆医科大学附属巴南医院,重庆401320

出  处:《实用中医内科杂志》2024年第1期37-40,I0004,I0005,共6页Journal of Practical Traditional Chinese Internal Medicine

基  金:国家自然科学基金项目(81860237)。

摘  要:谷氨酸作为一种神经递质,在中枢神经系统信号传递中起着重要作用。缺血性脑卒中引起大量神经递质释放可造成兴奋性氨基酸毒性,神经元持续性去极化造成细胞骨架破坏,引起各项神经功能障碍。中枢神经受损后会分泌大量神经再生抑制分子激活RhoA蛋白通路,导致生长锥塌陷,抑制神经突起再生。干预生长锥塌陷途径,减轻兴奋性氨基酸毒性造成的神经突起损伤和促进神经突起再生成为当今研究热点。文章对谷氨酸损伤神经突起机制及促进神经突起再生机制展开深入讨论。Glutamate as a neurotransmitter,plays an important role in signal transmission in the central nervous system.The release of a large number of neurotransmitters caused by ischemic stroke can cause excitatory amino acid toxicity,and the contin-uous depolarization of neurons can cause cytoskeleton damage and cause various neurological dysfunction.It is found that after the central nervous system is damaged,a large number of nerve regeneration inhibitory molecules will be secreted to activate the RhoA protein pathway,which will lead to the collapse of the growth cone and inhibit the regeneration of neurites.Intervening the collapse of growth cone,reducing neurite injury caused by excitatory amino acid toxicity and promoting neurite regeneration have become the focus of current research.In this paper,the mechanism of glutamate damaging neurites and promoting neurite regen-eration will be discussed in depth.

关 键 词:缺血性脑卒中 谷氨酸 RHOA 神经再生 

分 类 号:R255.2[医药卫生—中医内科学]

 

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