Received 2002-03-29 Accepted 2002-09-09
*Corresponding author.
氯化钴增强培养海马神经元葡萄糖转运活性参与抗缺氧作用
于顺2, 范明1*, 赵彤1, 丁爱石1, 王福庄1
1军事医学科学院基础医学研究所神经生物学研究室, 北京100083;
2首都医科大学宣武医院老年病研究所, 北京 100053
摘要: 本文在培养新生大鼠海马神经元观察了氯化钴对葡萄糖转运活性的影响及其在神经元抗缺氧中的作用。结果表明, 用CoCl2处理的培养海马神经元, 24 h后其2-脱氧-D-[1-3H]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8 h6-hour or 8-hour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。本文结果提示, 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。CoCl2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
中图分类号: R338;
R329.2+8
CoCl2 -induced enhancement of
glucose transport activity medinting hypoxic
tolerance in cultured
hippocampal
neurons
Yu Shun2, Fan Ming1, Zhao Tong1, Ding Ai-Shi1, Wang Fu-Zhuang1
1Department
of Neurobiology,
2Beijing
Abstract: The effect of CoCl2 pretreatment on glucose transport activity of the cultured newborn rat hippocampal neurons and its role in neuronal hypoxic tolerance were observed. The results showed that the 2-deoxy-D-[1-3H ]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 CoCl2. The cell injury induced by 6-hour or 8-hour hypoxic exposure was aiso greatly reduced by CoCl2 pretreatment. The protective effect of CoCl2 on the neurons was largely abolished by Cytochalasin B, a specific inhibitor of glucose transporters. The results suggest that CoCl2 can increase mRNA expressions of GLUT1 and GLUT3 and glucose transporter activity of the neurons, which may be the important mechanism for the increased tolerance of the neurons to hypoxia.
Key words: hypoxia; CoCl2; glucose transporter; neuron