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.
出处
《第四军医大学学报》
北大核心
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)
