17β-雌二醇对H_2O_2诱导视网膜神经细胞死亡的作用

目的　研究 17β 雌二醇 (βE2 )对培养的视网膜神经细胞的保护作用。方法　应用视网膜神经细胞培养的方法 ,观察H2 O2 、βE2以及雌激素受体阻断剂它莫西芬对视网膜神经细胞的作用。 结果　H2 O2 能显著降低培养的视网膜神经细胞的存活率 ,表现为剂量、时间依赖型。用 βE2预培养细胞 30min后 ,再加H2 O2 继续培养 2 4h细胞存活率明显上升 (P <0 .0 5 )。用它莫西芬预培养细胞后 ,重复上述实验 ,发现它莫西芬不能阻断 βE2的作用。免疫细胞化学鉴定原代细胞中 99%以上的细胞为雌激素受体阴性。结论　H2 O2 能导致培养的视网膜神经细胞的死亡。βE2能降低H2 O2 的毒性作用。它莫西芬不能阻断βE2的保护作用 ,培养的光受体细胞为雌激素受体阴性。提示 βE2的作用机制可能不是经雌激素受体介导的途经

Effects of 17β -estradiol on hydrogen peroxide-induced cell death in cultured retinal neurons

Objective To investigate the protective effect of 17β-estradiol (βE2) on cultured retinal neurons. Methods By using methods of the cultured retinal neurons, the effects of H 2O 2, β E2, and tamoxifen, the estrogen receptor antagonist, on the cultured retinal neurons were observed. Results H 2O 2 significantly decreased cell viability in cultured retinal neurons in a dose- and time-dependent manner. When the retinal neurons were pretreated with β E2 30 min prior to H 2O 2 treatment, cell viability was significantly increased (P< 0.05). Pretreatment with tamoxifen for 30 min prior to the addition of β E2 did not significantly block the neuroprotective effect of β E2. Immunocytochemical analysis of cultured primary retinal neurons showed that a large proportion of cells (more than 99%) was estrogen receptor negative. Conclusion H 2O 2 can significantly induce cell death in cultured retinal neurons and pretreatment of the cells with βE2 inhibits this process. However, tamoxifen does not significantly attenuate the protection provided by βE2, and estrogen receptors cannot be detected in photoreceptor cell. These results suggest that neuroprotective effects of βE2 do not involve activation of estrogen receptors.