华东师范大学学报(自然科学版) ›› 2004, Vol. 2004 ›› Issue (3): 121-125,.

• 生命科学 • 上一篇    下一篇

枸杞多糖对四氯化碳和高糖致损大鼠肝细胞的作用

张红锋, 徐曼艳, 王耀发   

  1. 华东师范大学 生命科学学院， 上海 200062
  • 收稿日期:2003-09-05 修回日期:2003-10-08 出版日期:2004-09-25 发布日期:2004-09-25
  • 通讯作者: 张红锋

Protective Effects of Lycium Bararum Polysaccharides on Carbon Tetrachloride and High Glucose Damaged Hepatocytes

ZHANG Hong-feng , XU Man-yan, WANG Yao-fa   

  1. Department of Biology, East China Normal University, Shanghai 200062, China
  • Received:2003-09-05 Revised:2003-10-08 Online:2004-09-25 Published:2004-09-25
  • Contact: ZHANG Hong-feng

摘要： 在四氯化碳(CCL4)和高糖(HG)损伤的离体肝细胞模型上，研究CCL4和HG对肝细胞葡萄糖激酶活性、钙离子浓度以及酪氨酸磷酸化水平的影响，并对枸杞多糖（LBP）的保护作用进行探讨.实验结果表明，CCL4和HG均使肝细胞内葡萄糖激酶活性下降，Ca超载，并使细胞内酪氨酸磷酸化水平降低.LBP可以改善CCL4和HG引起的葡萄糖激酶活性和钙离子浓度的变化，以及CCL4引起的胰岛素信号通路中的酪氨酸激酶活性的下降，但不能改善高糖引起的酪氨酸激酶活性的下降.由此认为，LBP对受到自由基直接损伤的肝细胞有较好的保护作用，而对高糖环境引起的肝细胞损伤不能完全修复，这可能与CCL4和HG的作用机制不同有关.

关键词: 四氯化碳, 高糖, 葡萄糖激酶, Ca2+, 酪氨酸磷酸化水平, 四氯化碳, 高糖, 葡萄糖激酶, Ca2+, 酪氨酸磷酸化水平

Abstract: Hepatocytes in vitro damaged by carbon tetrachloride (CCL4) and high glucose(HG) were used to research the mechanism of CCL4 and HG on the glucokinase(GK) activity,the intercellular Ca2+ concentration and the level of tyrosine phosphorylation in cells ,and then the protective effects of Lycium bararum polysaccharides(LBP).The results showed that CCL4 and HG inhibited the GK activity,elevated Caconcentration and decreased the level of tyrosine phosphorylation in hepatocytes. LBP could improve the change of the GK activity and Ca2+ concentration induced by CCL4 and HG, and the decrease of tyrosikinase activity in the pathway of insulin induced by CCL4 only.But LBP couldn’t improve the decrease of tyrosikinase activity induced by HG.The conclusion was that LBP could protect hepatocytes against free radicals directly,but not against the damage of HG. This related to the different mechanism of CCL4 and HG.

Key words: high glucose, glucokinase, Ca2+, the level of tyrosine phosphorylation, carbon tetrachloride, high glucose, glucokinase, Ca2+, the level of tyrosine phosphorylation

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