中国老年学杂志
中國老年學雜誌
중국노년학잡지
CHINESE JOURNAL OF GERONTOLOGY
2009年
24期
3199-3201
,共3页
张志慧%周龙岗%王玲玲%葛小丽%魏聪
張誌慧%週龍崗%王玲玲%葛小麗%魏聰
장지혜%주룡강%왕령령%갈소려%위총
Aβ淀粉样蛋%通心络%神经元凋亡%caspase-3%凋亡相关基因蛋白
Aβ澱粉樣蛋%通心絡%神經元凋亡%caspase-3%凋亡相關基因蛋白
Aβ정분양단%통심락%신경원조망%caspase-3%조망상관기인단백
β-amyloid protein%Tongxinluo%Neuron apoptosis%Caspase-3%Apoptosis-associated gene
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Aβ_(1-42)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.
目的 探討Aβ誘導皮層神經元凋亡的機製及通心絡的榦預作用.方法 原代培養的小鼠皮層神經,經Aβ1-42處理後,MTT判斷神經元存活率,Hoechst33342染色、流式細胞儀檢測檢測神經元凋亡,Western印跡法檢測caspase凋亡蛋白的錶達.結果 神經元經Aβ_(1-42)處理後,活細胞數減少,染色質濃縮、覈碎裂,染色暘性神經元增多,細胞凋亡率上升,caspase-3錶達增彊.通心絡可明顯改善上述變化.結論 Aβ通過caspase-3途徑引起神經元凋亡從而導緻神經元細胞死亡.通心絡可抑製Aβ誘導的神經元凋亡來保護神經元,從而起到治療AD的作用.
목적 탐토Aβ유도피층신경원조망적궤제급통심락적간예작용.방법 원대배양적소서피층신경,경Aβ1-42처리후,MTT판단신경원존활솔,Hoechst33342염색、류식세포의검측검측신경원조망,Western인적법검측caspase조망단백적표체.결과 신경원경Aβ_(1-42)처리후,활세포수감소,염색질농축、핵쇄렬,염색양성신경원증다,세포조망솔상승,caspase-3표체증강.통심락가명현개선상술변화.결론 Aβ통과caspase-3도경인기신경원조망종이도치신경원세포사망.통심락가억제Aβ유도적신경원조망래보호신경원,종이기도치료AD적작용.
Objective To study the mechanism ofβ-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.
