17β-Estradiol protects SD rat retinal neurons from light damage by activating PI3K/Akt and NF-κB signal pathways
作者单位：Department of Genetics and Molecular BiologySchool of MedicineXi’an Jiaotong University
会议名称：《中国生物化学与分子生物学会第十届会员代表大会暨全国学术会议》
会议日期：2010年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 10[医学]
关 键 词：17β-estradiol retinal light damage neuroprotection apoptosis
摘 要：Our previous studies have proved that the phosphatidylinositol-3-kinase(PI3K)/Akt signal pathway was involved in the neuroprotection of 17β-estradiol(βE2) against H2O2-induced retinal neurons apoptosis in *** aim of this study is to observe whetherβE2 can also protect retinal neurons from light damage in vivo by activating the PI3K/Akt signal *** used 180 to 230 g female SD rats exposed to persistent white light after ovariectomy 2 weeks as experimental model and used Electroretinogram (ERG),DNA ladder,TUNEL,HE staining,Western blotting and Immunofluorescence techniques to investigate the neuroprotection ofβ*** results showed that SD rats were exposed to 8000 lux white light for 12 h resulted in retinal function decrease and photoreceptor cells apoptosis, and 10-4M and 10-5MβE2 by intravitreal injection all significantly enhanced the photosensitive function of retinal by preventing neuronal *** mechanism research found that the neuroprotection ofβE2 involved in increasing the phosphorylation of Akt which was partly blocked by the pretreatment with PI3K inhibitor LY294002 for 30 min beforeβE2 *** cleaved caspase-3 as an activation form of caspase-3 was observed after light damage and the administration ofβE2 can attenuate the activation of caspase-3,while pretreatment with LY294002 can inhibit the attenuation ofβ*** results showed that NF-κB translocated from cytoplasm to nucleus afterβE2 injection,and LY294002 could also inhibit partly this *** present results indicated thatβE2 has a neuroprotective effect against light-induced photoreceptor cells apoptosis,and the PI3K/Akt pathway plays an important role in this neuroprotection,which involved in translocation of NF-κB from cytoplasm to nucleus and inhibited the activation of caspase- 3,but the detailed mechanism of theβE2 neuroprotection is being further study.