The role of Toll-like receptor 2 and down streaming signaling in opioids-mediated apoptosis

LI Yi; et al

doi:10.13406/j.cnki.cyxb.2010.09.027

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The role of Toll-like receptor 2 and down streaming signaling in opioids-mediated apoptosis

更新时间：2024-01-17

- The role of Toll-like receptor 2 and down streaming signaling in opioids-mediated apoptosis
- Journal of Chongqing Medical University Vol. 35, Issue 9, Pages: 1289-1294(2010)
- 作者机构：
  
  中山大学附属第二医院神经内科
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2010.09.027
  CLC： R749.6
- Published：2010，
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[1]李艺,彭英.Toll-like receptor 2及其信号传导通路在阿片类物质诱导细胞凋亡中的作用[J].重庆医科大学学报,2010,35(09):1289-1294.

LI Yi, et al. The role of Toll-like receptor 2 and down streaming signaling in opioids-mediated apoptosis. [J]. Journal of Chongqing Medical University 35(9):1289-1294(2010)
[1]李艺,彭英.Toll-like receptor 2及其信号传导通路在阿片类物质诱导细胞凋亡中的作用[J].重庆医科大学学报,2010,35(09):1289-1294. DOI： 10.13406/j.cnki.cyxb.2010.09.027.

LI Yi, et al. The role of Toll-like receptor 2 and down streaming signaling in opioids-mediated apoptosis. [J]. Journal of Chongqing Medical University 35(9):1289-1294(2010) DOI： 10.13406/j.cnki.cyxb.2010.09.027.

摘要

目的:成瘾物质（Addictive drugs）导致的中毒性脑病的中枢神经系统损害以神经元凋亡为突出表现

具体机制仍有待进一步的研究探讨。方法:Toll-like receptor 2（TLR2）不仅是激活机体自身免疫防御和炎症反应的重要受体

而且广泛参与多种细胞功能

包括细胞凋亡。我们使用体外培养的HEK293和高表达TLR2的HEK2932种细胞

以及体外培养小鼠皮层原代神经元细胞

研究经过吗啡处理后细胞存活率和凋亡的变化

以探讨TLR2信号通路在吗啡诱导的细胞凋亡中的作用。结果:TLR2高表达导致吗啡诱导的细胞存活率下降和细胞凋亡的显著增加。使用MyD88抑制体竞争性抑制MyD88并阻断TLR2信号通路后

吗啡诱导的TLR2高表达细胞的凋亡也被明显抑制。长期的吗啡处理导致正常神经元的TLR2在信使RNA（mRNA）水平和蛋白水平表达明显增高

而且在TLR2功能缺失的原代神经元细胞中

吗啡诱导的caspase-3活性增高被阻断

吗啡诱导的神经元凋亡也被明显抑制。结论:TLR2信号通路参与吗啡诱导的神经元凋亡。

Abstract

Objective:Toxicenc ephalopathy caused by addictive substances

during which the neuron apoptosis was recognized as the outstanding performance in central nervous system damage

however the specific mechanisms still need further study.Methods:Toll-like receptor 2(TLR2)is not only activate the body’s own immune defense and the important receptors in inflammation

but also be broad participation in a variety of cell functions

including apoptosis.The three kinds cells

HEK293 cultured in vitro

HEK293 which highly expressed TLR2 cultured in vitro and primary cultured cortical neurons of mice were employed to studied the cell survival rate and apoptosis after handled by morphine

further more to explore the function of TLR2 signaling pathway in cell apoptosis caused by morphine.Results:The results showed that

highly TLR2 expression of morphine-induced cells led to decreased survival and apoptosis increased significantly.MyD88 suppression was used to in competitive inhibition of MyD88 and block TLR2 signaling pathway

then the morphine-induced TLR2 highly expression cell apoptosis was significantly inhibited.Long-term morphine treatment resulted in normal neurons in the mRNA level of TLR2 expression and protein levels were significantly higher

and that TLR2 function in the absence of primary neuron cells

morphine-induced increase of caspase-3 activity was blocked and morphine-induced nerve Apoptosis is also inhibited.Conclusion:The results show that TLR2 signaling pathway is involved in morphine-induced neuronal apoptosis.

关键词

中毒性脑病Toll-like receptor 2吗啡凋亡

Keywords

Addictivedrugs-toxicencephalopathyToll-likereceptor2Morphineapoptosis

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