The effect of polypyrimidine tract binding protein-associated splicing factor on hydrogen peroxide induced apoptosis of retinal pigment epithelial
10.3760/cma.j.issn.1005-1015.2018.02.012
- VernacularTitle:聚嘧啶束结合蛋白相关剪接因子对过氧化氢诱导下视网膜色素上皮细胞凋亡的影响
- Author:
Fang TIAN
1
;
Wenbo LI
;
Liangyu HUANG
;
Meizi GAO
;
Jinzhi ZHAO
;
Bojie HU
;
Xiaomin ZHANG
;
Xiaorong LI
;
Lijie DONG
Author Information
1. 300384,天津医科大学眼科医院天津医科大学眼科研究所天津医科大学眼视光学院
- Keywords:
Retinal pigment epithelium;
Polypyrimidine tract-binding protein;
Apoptosis;
Hydrogen peroxide
- From:
Chinese Journal of Ocular Fundus Diseases
2018;34(2):159-163
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect ofpolypyramidine tract binding protein-associated splicing factor (PSF) on hydrogen peroxide (H2O2) induced apoptosis of retinal pigment epithelial (RPE) cells in vitro.Methods RPE cells were cultured and divided into a normal group,normal+H2O2 group,Vec+H2O2 group,PSF+H2O2 group according to the experimental design.Overexpression of PSF in RPE cells were achieved by pEGFP-PSF plasmid transient transfection into RPE cells,then RPE cells were exposed to H2O2.The morphological changes were observed by hematoxylin-eosin (HE) staining and Live/Dead staining while the survival rate of cells was detected by MTT assay.The effect of PSF on H2O2-induced RPE apoptosis was analyzed by Cell Death Detection ELISA kit.Meanwhile,intracellular reactive oxygen species (ROS) level was detected by using DCFH-DA method.Results Overexpression of PSF could effectively alleviate the morphological changes induced by H2O2 stimulation shown by HE staining,and effectively reduce dead cells number shown by Live/Dead staining.After H2O2 stimulation,the survival rate,apoptosis rate and ROS production level in PSF overexpression group were 0.68± 0.12,0.44± 0.08 and 18 616± 3 382.54 respectively,showing significant difference in comparison with the vector plasmid group and normal group (P＜0.05).Conclusion PSF overexpression plays a protective role in H2O2-induced apoptosis by inhibiting the production of ROS in RPE cells.
