摘要
目的探讨Aβ诱导皮层神经元凋亡的机制及通心络的干预作用。方法原代培养的小鼠皮层神经,经Aβ1-42处理后,MTT判断神经元存活率,Hoechst33342染色、流式细胞仪检测检测神经元凋亡,Western印迹法检测caspase凋亡蛋白的表达。结果神经元经Aβ1-42处理后,活细胞数减少,染色质浓缩、核碎裂,染色阳性神经元增多,细胞凋亡率上升,caspase-3表达增强。通心络可明显改善上述变化。结论Aβ通过caspase-3途径引起神经元凋亡从而导致神经元细胞死亡。通心络可抑制Aβ诱导的神经元凋亡来保护神经元,从而起到治疗AD的作用。
Objective To study the mechanism of β-amyloid （Aβ） on neuron apoptosis and the effect of Tongxinluo. Methods The neuron survival, apoptosis of neurons were detected by Hoechst 33 342 staining, the expression pf caspase-3 was determined by Western blot. Results The number of viable cells was decreased and the condensation of chromatin and nuclear fragmentation were shown after Aβ1 - 42 treatment. The expression of caspase-3 was elevated after treated with Tongxinluo, all the above indexes were improved. Conclusions The mechanism of Aβ1-42 inducing neuron apoptosis is related to its regulation on the expression of apoptosis-associated gene and the caspase-3 pathway. Tongxinluo could attenuate the neurotoxic action of Aβ1-42 and improve neuron survival.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2009年第24期3199-3201,共3页
Chinese Journal of Gerontology
基金
国家重点基础研究发展计划(973计划)项目(2005CB523301)
