第Ⅲ组代谢型谷氨酸受体拮抗Aβ 31-35诱导神经元凋亡的机制探讨  

Mechanisms of group Ⅲ mGluRs against cultured neuron apoptosis induced by β-amyloid peptide 31-35

作　　者：赵丽[1,2] 崔爱玲[3] 张策[1] 

机构地区：[1]山西医科大学,山西太原030001 [2]北京体育大学,北京100084 [3]新乡医学院,河南新乡453003

出　　处：《第四军医大学学报》2009年第24期2931-2934,共4页Journal of the Fourth Military Medical University

基　　金：国家自然科学基金(30572085);教育部新教师基金(200800431001)

摘　　要：目的:探讨第Ⅲ组代谢型谷氨酸受体(mGluRs)拮抗Aβ31-35诱导神经元凋亡的机制.方法:原代培养的大鼠额叶皮层神经元,加入第Ⅲ组mGluRs激动剂L-SOP或(R,S)-PPG,利用流式细胞仪和caspase酶系活性检测观察对Aβ31-35诱导神经元凋亡的影响.结果:第Ⅲ组mGluRs激动剂L-SOP或(R,S)-PPG明显抑制Aβ31-35引起的凋亡,其caspase-3活性降低,同时参与内源性凋亡的caspase-9和外源性凋亡的caspase-8活性均明显降低.结论:第Ⅲ组mGluRs激动剂通过内、外两条途径抑制Aβ31-35诱导的神经元凋亡.AIM：To determine the mechanisms of neuroprotection by group III metabotropic glutamate receptors（mGluRs） activation against apoptosis induced by β-amyloid peptide 31-35（Aβ31-35） in frontal lobe cortical neurons.METHODS：The cerebral cortical neurons were incubated with Aβ31-35（25 μmol/L） or coapplied with group III mGluRs agonist of L-SOP or（R,S）-PPG（100 μmol/L） for 24 h.The apoptosis of the cells was analyzed by flow cytometry and caspases activity.RESULTS：L-SOP or（R,S）-PPG（100 μmol/L） significantly inhibited the neuron apoptosis and decreased caepase-3,-8 and-9 in the Aβ31-35 treated neurons.CONCLUSION：The results described in the present study suggested that activation of group III mGluRs protected neurons from Aβ31-35-induced apoptosis by blocking the caspase-dependent intrinsic and extrinsic apoptotic pathways.

关 键 词：Aβ31-35 caspases活性 第Ⅲ组mGluRs 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]