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脑出血后继发海马神经元损伤的机制研究进展

Research progress on the mechanism of secondary hippocampal neuronal injury after intracerebral hemorrhage

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【作者】 王雪; 朱业淘; 徐剑峰; 王童; 刘阳;

【Author】 WANG Xue;ZHU Yetao;XU Jianfeng;WANG Tong;LIU Yang;Mianyang Third People’s Hospital/Sichuan Mental Health Center;Affiliated Hospital of Southwest Medical University;

【通讯作者】 刘阳;

【机构】 绵阳市第三人民医院(四川省精神卫生中心); 西南医科大学附属医院;

【摘要】 脑出血是一种致死率、致残率较高的疾病,除造成血肿周围损伤外,还可致远端脑区损伤及其功能发生变化,例如脑出血可致海马结构和功能发生改变,包括神经细胞坏死、突触可塑性破坏,炎症因子表达增加,谷氨酸大量释放,以及N-甲基-D-天冬氨酸受体(NMDAR)过度激活等。海马神经元损伤与脑出血后继发性损伤机制相关,目前脑出血后继发性损伤机制存在多种说法,如谷氨酸兴奋性毒性、自噬激活、炎症、氧化应激以及铁超载等。这些机制的研究为脑出血后海马神经元损伤所致认知功能障碍的治疗奠定相关理论基础,推动脑出血后认知障碍治疗的发展。

【Abstract】 Intracerebral hemorrhage is a disease with high fatality and disability.In addition to surrounding hematoma injury,intracerebral hemorrhage can also lead to distal brain injury and functional changes.For example,intracerebral hemorrhage can cause changes in hippocampal structure and function,including nerve cell necrosis,synaptic plasticity destruction,increased expression of inflammatory factors,massive release of glutamate,and the overactivation of N-methyl-D-aspartate receptor(NMDAR).Hippocampal neuron injury is related to the secondary injury mechanism after intracerebral hemorrhage.Currently,there are many theories about the secondary injury mechanism after intracerebral hemorrhage,such as glutamate excitatory toxicity,autophagy activation,inflammation,oxidative stress and iron overload.The study of these mechanisms lays a theoretical foundation for the treatment of cognitive dysfunction caused by hippocampal neuron damage after intracerebral hemorrhage,and promotes the development of the treatment of cognitive dysfunction after intracerebral hemorrhage.

【基金】 四川省医学会科研项目(编号:S22007,S21073);绵阳市第三人民医院科研项目(编号:202219)
  • 【文献出处】 中国实用神经疾病杂志 ,Chinese Journal of Practical Nervous Diseases , 编辑部邮箱 ,2023年11期
  • 【分类号】R743.34
  • 【下载频次】11
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