| 摘要: |
| ［摘要］ 脑水肿是脑出血后常见的病理过程，可分为细胞毒性脑水肿和血管源性脑水肿；脑水肿程度在脑出血继发性脑神经损伤的机制中占有非常重要的地位。AQP-4作为转运水及某些小分子物质的通道，可加重细胞毒性脑水肿，减轻血管源性脑水肿，其机制可能与AQP-4表达的空间特异性和时间依赖性有关。Ca2+作为细胞内第二信使，参与神经递质的合成与释放，其含量增高可加重脑水肿并使AQP-4表达上调，而AQP-4亦可作为信号通路对Ca2+起着调节作用。该文综述了近几年来AQP-4和Ca2+与脑出血后脑水肿关系的相关研究进展。 |
| 关键词: AQP-4 Ca2+ 脑出血 脑水肿 |
| DOI：10.3969/j.issn.1674-3806.2013.01.30 |
| 分类号:R 742 |
| 基金项目:湖南省自然科学基金资助项目（编号：10JJ6050）；湖南省科学技术基金资助项目（编号：2011SK3100） |
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| Research progress of effect of AQP-4 and Ca2+ on brain edema induced by cerebral hemorrhage |
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ZHOU De-sheng,LIU Li-juan,CHEN Yao,et al.
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Department of Neurology, the First Affiliated Hospital to Hunan Chinese Medical University,Changsha 410007,China
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| Abstract: |
| ［Abstract］ Brain edema induced by intracerebral hemorrhage is a common pathology process which can be divided into cell toxicity brain edema and vasogenic brain edema. The degree of edema occupied a very important position in the mechanism of cranial nerve damage secondary to cerebral hemorrhage.AQP-4 as transport passage of water and some small molecules channels, may increase cell toxicity brain edema, reduce vasogenic brain edema.Its mechanism may be related to the space specificity and time-dependence of the expression AQP-4. Ca2+ as a second messenger in cells, participates in the neurotransmitter’s synthesis and release, the increase of its content can increase brain edema and make AQP-4 expression rising. AQP-4 as a signal access may also play a role in regulation of Ca2+. This paper reviewed the relevant research in recent years. |
| Key words: Aquaporin-4 Ca2+ Cerebral hemorrhage Brain edema |
