摘要
目的 探讨维生素E(VitE)拮抗 β淀粉样蛋白2 5 3 5(Aβ2 5 3 5)对神经细胞株SH SY5Y的损伤 ,即VitE保护神经细胞的机制。 方法 采用流式细胞法、反转录PCR法研究VitE对SH SY5Y细胞的保护作用及机制。 结果 对照组细胞凋亡率为 ( 3 6 0± 0 37) % ,Aβ2 5 3 5处理组细胞凋亡率为 ( 39 15± 3 14 ) % ,VitE和Aβ2 5 3 5共同处理组细胞凋亡率为 ( 17 89± 2 0 7) % ;对照组细胞内Ca2 +为 ( 2 76± 0 2 1) % ,Aβ2 5 3 5处理组细胞内Ca2 +为 ( 13 70± 1 4 5 ) % ,VitE和Aβ2 5 3 5共同处理组细胞内Ca2 +为 ( 9 6 1± 1 0 2 ) %。经VitE和Aβ2 5 3 5共同处理的SH SY5Y细胞 ,其反转录PCR产物的凝胶电泳中 ,caspase 3与管家基因 β actin的比为 0 76 ,而单纯Aβ2 5 3 5处理组caspase 3与 β actin的比为 0 99。 结论 Aβ2 5 3 5促使SH SY5Y细胞凋亡和Ca2 +超载 ,并伴caspase 3在转录水平增高 ;而VitE能拮抗上述各环节 ,从而保护SH
Objective To investigate the mechanism of Vit E inhibiting effect on the damage of neurocytes caused by Aβ 25 35 . Methods Flow cytometry was employed to determine the apoptosis of neurocytes and calcium overloading. The level of mRNA of caspase 3 was indirectly measured by RT PCR Results Vit E inhibited the apoptosis of SH SY5Y cells and decreased the calcium over loading caused by Aβ 25 35 . The apoptotic rate of the control group was (3 60±0 37)%, of the Aβ 25 35 treated group was (39 15±3 14)%,and of the Vit E and Aβ 25 35 co treated group was (17 89±2 07)%. The calcium concentration of the control group, the Aβ 25 35 treated group and the Vit E and Aβ 25 35 co treated group was (2 76±0 21)%, (13 70±1 45)%, (9 61±1 02)%, respectively. RT PCR result showed lower level of caspase 3 in Vit E and Aβ 25 35 co treated group(0 76) than the Aβ 25 35 treated group(0 99). Conclusions Aβ 25 35 improved apoptosis and the calcium over loading of the SH SY5Y cells, and increased the expression of caspase 3 at the transcript level; and Vit E can inhibit the damage caused by Aβ 25 35 .
出处
《中华老年医学杂志》
CAS
CSCD
北大核心
2004年第10期718-720,共3页
Chinese Journal of Geriatrics
