摘要
目的:研究17β雌二醇(βE2)保护视网膜神经细胞的作用与磷脂酰肌醇3激酶(PI3K)的活性关系.方法:应用视网膜神经细胞培养、MTT测定、PI3K活性测定及Western blot分析的方法,观察βE2与视网膜神经细胞PI3K的关系.结果:10μmol/LβE2培养细胞30min后,PI3K的活性开始上升,1h达高峰,12h恢复正常.用βE2直接与细胞匀浆37℃孵育1h,PI3K活性没有改变.而且βE2也未影响PI3K在细胞中的表达.PI3K抑制剂LY294002降低了βE2削弱H2O2的毒性作用.结论:βE2能间接激活细胞中PI3K的活性,LY294002抑制了βE2保护视网膜神经细胞的作用.提示βE2的神经保护作用可能与PI3K的激活有关.
AIM: To investigate the relationship between the retinal neuroprotective effect of βE2 and the activity of PI3K. METHODS: The relationship between the retinal neuroprotective effect of βE2 and activity of PI3K was investigated by methods of cultured retinal neurons, MTT assay, PI3K assay and Western blot analysis. RESULTS: PI3K activity was increased by a 30 min treatment of cultured retinal neurons with 10 μmol/L βE2 and reached a plateau at 1 h. The PI3K activity returned to control level after 12 h. The incubation of βE2 directly with a homogenate of cultured retinal neurons did not activate PI3K and the expression of PI3K did not respond to βE2 treatment. LY294002, a PI3K inhibitor, greatly inhibited the βE2 attenuated H 2O 2-induced cytotoxicity. CONCLUSION: βE2 can significantly activate PI3K in cells in an indirect way and LY294002 can significantly inhibit the retinal nueroprotection provided by βE2, suggesting that neuroprotective effects of βE2 are related to the activation of PI3K.
出处
《第四军医大学学报》
北大核心
2005年第9期808-811,共4页
Journal of the Fourth Military Medical University