β淀粉样蛋白25-35致神经细胞损伤的机制及信号转导通路初步研究  

Mechanism of Cell Damage Caused by Aβ25-35 and Study of Signal Transduction

作　　者：刘江红[1] 许贤豪[2] 黎健[3] 唐蔚青[3] 彭丹涛[2] 孟晓梅[2] 褚德发[4] 

机构地区：[1]首都医科大学宣武医院神经内科,北京100053 [2]卫生部北京医院神经内科,北京100730 [3]卫生部北京医院老年医学研究所生化室,北京100730 [4]卫生部北京医院统计室,北京100730

出　　处：《中国神经免疫学和神经病学杂志》2006年第3期129-132,i0001,共5页Chinese Journal of Neuroimmunology and Neurology

摘　　要：目的探讨β淀粉样蛋白25-35(Aβ25-35)导致神经细胞损伤的机制及在损伤过程中涉及的信号转导通路中相关酶caspase-3的变化。方法采用荧光染色法、流式细胞法、反转录PCR法研究Aβ25-35对SH-SY5Y细胞的损伤机制及信号转导通路中caspase-3的变化。结果经Aβ25-35处理的SH-SY5Y细胞核中出现浓染的碎块状荧光,流式细胞法检测到凋亡特有的亚二倍体峰,对照组细胞凋亡率为(3.57±0.28)%(n=9),经10、20μmol/L Aβ25-35处理30 h的细胞,其凋亡率分别为(17.44±1.27)%和(38.82±2.06)%,与对照组比较差异有统计学意义(均P<0.01)。反转录PCR产物凝胶电泳的caspase-3与看家基因-βactin的比(0.92)高于对照组(0.19)。结论Aβ25-35促使SH-SY5Y细胞凋亡,此过程中caspase-3转录水平增高。Objective To investigate the mechanism of neurocytes＇ damage caused by Aβ25-35 and the change of enzyme in the signal transduction passway. Methods The methods such as fluorescence dying, flow-eytometry and RT-PCR were used. Results After treated by Aβ25-35, there was dense fluorescence fragment in the nucleus of the SH-SYSY cells, through flow-cytometry, the sub-diploid peak could be seen the apoptosis rate of the control, the cells treated with 10 μmol/L and 20 μmol/L Aβ25-35 for 30 hours was （3.57±0. 28）% （n= 9）, （17.44±1.27） % （P〈0. 01） and （38. 82 ± 2.06） % （P〈0. 01） respectively. The result of RT-PCR showed the percentage of caspasc-3 was higher in treated group （0. 92） than that in the control group（0. 19）. Conclusions Aβ25-35 increased the apoptosis of the SH-SYSY cells and the expression of caspase-3 transcript level.

关 键 词：AΒ25-35 凋亡 信号转导 CASPASE-3 

分 类 号：R749.1[医药卫生—神经病学与精神病学]