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氯化钴增强培养海马神经元葡萄糖转运活性参与抗缺氧的作用

于顺, 范明, 赵彤, 丁爱石, 王福庄

首都医科大学宣武医院老年病研究所.北京 100053；军事医学科学院基础医学研究所神经生物学研究室.北京 100850

摘要

用CoCl_(2)处理的培养海马神经元,24h后其2-脱氧-D-[1-~(3)H]葡萄糖摄取率和葡萄糖转运体GLUT1和GLUT3 mRNA表达明显高于对照组,并且其在缺氧6或8h后的损伤也明显减轻。氯化钴对神经元缺氧损伤的保护作用被葡萄糖转运体抑制剂细胞松弛素B大部分消除。结果提示,氯化钴能够增强神经元GLUT1和GLUT3 mRNA的表达和葡萄糖转运活性。CoCl_(2)的这一作用可能是其增强神经元抗缺氧的重要机制。

关键词： 缺氧; 氯化钴; 葡萄糖转运体; 神经元

CoCl_(2)-induced enhancement of glucose transport activity in mediating hypoxic tolerance in cultured hippocampal neurons

Yu Shun, Fan Ming, Zhao Tong, Ding Aishi, Wang Fuzhuang

Beijing Institute of Geriatrics,Xuanwu Hospital of Capital University of Medical Sciences.Beijing 100053；China

Abstract

The results showed taht the 2-deoxy-D-[1-~(3)H] glucose uptake rate and the mRNA expressions of glucose transporters (GLUT1 and GLUT3) in the hippocampal neurons were significantly increased after a 24-hour pretreatment with CoCl_(2). The cell injury induced by 6-hour or 8-hour hypoxic exposure was also greatly reduced by CoCl_(2) pretreatment. The protective effect of CoCl_(2) on the neurons was largely abolished by cytochalasin B, a specific inhibitor of glucose transporters. The results suggest that CoCl_(2) can increase mRNA expressions of GLUT1 and GLUT3 and glucose transporter activity of the neurons, which may be an important mechanism for the increased tolerance of the neurons to hypoxia.

Key words: Hypoxia;CoCl_(2);Glucose transporter;Neuron

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引用本文：

于顺, 范明, 赵彤, 丁爱石, 王福庄. 氯化钴增强培养海马神经元葡萄糖转运活性参与抗缺氧的作用[J]. 生理学报 2002; 54 (6): .

Yu Shun, Fan Ming, Zhao Tong, Ding Aishi, Wang Fuzhuang. CoCl_(2)-induced enhancement of glucose transport activity in mediating hypoxic tolerance in cultured hippocampal neurons. Acta Physiol Sin 2002; 54 (6): (in Chinese with English abstract).