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
赵丽 1崔爱玲 2张策3
作者信息
- 1. 山两医科大学,山西,太原,030001;北京体育大学,北京,100084
- 2. 新乡医学院,河南,新乡,453003
- 3. 山两医科大学,山西,太原,030001
- 折叠
摘要
目的:探讨第Ⅲ组代谢型谷氨酸受体(mGluRs)拮抗AB 31-35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Aβ 31-35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Ap 31-35诱导的神经元凋亡.
Abstract
AIM:To determine the mechanisms of neuroprotection by group Ⅲ metabotropic glutamate receptors(mGluRs)activation against apoptosis induced by 13-amyloid peptide 31-35 (Aβ31-35)in frontal lobe cortical neurons.METHODS:The cerebral cortical neurons were incubated with A1331-35(25 μmol/L)or coapplied with group Ⅲ mGluRs agonist of L-SOP or(R,S)PPG(100μmol/L)for 24 h.The apoptosis of the cells was analyzed by flow cytometry and easpases 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 Aμ31-35 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
AB/31-35/caspases活性/第Ⅲ组mGluRsKey words
Aβ31-35/caspases activity/group Ⅲm GluRs引用本文复制引用
基金项目
国家自然科学基金(30572085)
教育部新教师基金(200800431001)
出版年
2009
NETL
NSTL
维普
万方数据