蝙蝠葛碱拮抗缓激肽引起的钙稳态改变 及细胞骨架蛋白的异常磷酸
DOI:
作者:
作者单位:

作者简介:

通讯作者:

中图分类号:

基金项目:

国家自然科学基金资助项目(30430270,30328007).


Dauricine Prevents Bradykinin-induced Alteration of Calcium Homeostasis and tau Hyperphosphorylation in N2a Cells
Author:
Affiliation:

Fund Project:

This work was supported by a grant from The National Natural Science Foundatin of China (30430270, 30328007).

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    为研究蝙蝠葛碱 (dauricine , Dau) 拮抗缓激肽 (bradykinin , BK) 诱导的 Alzheimer 样钙稳态失衡及细胞骨架蛋白异常磷酸化的作用,采用双波长荧光分光光度计测定细胞内钙离子浓度 ([Ca2+] i) ,用 MTT 法检测细胞代谢水平,用免疫组织化学方法观察 tau 蛋白表达和磷酸化 . 结果表明,Dau (3 μmol/L , 6 μmol/L) 可抑制 BK 诱导的 [Ca2+]i 升高,保护 BK 引起的神经元代谢降低,拮抗 BK 引起的 tau 蛋白异常磷酸化和聚集 . 结果提示: Dau 可拮抗 BK 诱导的 Alzheimer 样钙稳态失衡及细胞骨架蛋白异常磷酸化的作用 .

    Abstract:

    To study the prevention of dauricine (Dau) on bradykinin (BK) induced alteration of intracellular calcium homeostasis and tau phosphorylation, fluorescence spectrophotometer with dual excitation was utilized to measure the intracellular calcium concentration ([Ca2+]i), MTT to detect cell viability and immuncytochemistry to examine tau phosphorylation. The results showed (1) cells treated with BK 1 μmol/L induced a transit increase in [Ca2+]i in all the cell lines detected, among them, the sustained increase of [Ca2+]i level was only seen in PS1 Δ9/APPswe cell at 2 h and 24 h after the treatment. Dau (3 μmol/L or 6 μmol/L) prevented BK-induced transit and sustained elevation and fluctuation of [Ca2+]i; (2) BK treatment decreased the cell metabolism detected at 2 h in PS1Δ9/APPswe and Dau antagonized the effect; (3) BK induces Alzheimer-like tau hyperphosphorylation at tau-1 epitope and Dau partially antagonized this effect. In conclusion, Dau inhibits BK-induced disturbance in intracellular calcium homeostasis and tau hyperphosphorylation at tau-1 sites.

    参考文献
    相似文献
    引证文献
引用本文

王乐,王小川,李宏莲,王丹玲,周新文,王建枝.蝙蝠葛碱拮抗缓激肽引起的钙稳态改变 及细胞骨架蛋白的异常磷酸[J].生物化学与生物物理进展,2005,32(7):612-617

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:
  • 最后修改日期:
  • 接受日期:
  • 在线发布日期:
  • 出版日期: