Expression of Fas/FasL ligand and cell apoptosis in ischemia/reperfusion-induced retina and effects of bFGF
- VernacularTitle:Fas/FasL系统在大鼠视网膜缺血再灌注凋亡损伤中的作用及bFGF的影响
- Author:
Ying, ZHAO
;
Ying-Jun, NIU
;
Zhan-Yu, ZHOU
;
Yun-Xia, GAO
;
Hong-Yun, WANG
- Publication Type:Journal Article
- Keywords:
retina;
ischemia/reperfuslon injury;
apoptosis;
fibroblast growth factor,basic;
Fas/FasL
- From:
International Eye Science
2005;5(3):423-427
- CountryChina
- Language:Chinese
-
Abstract:
· AIM: To explore the relationship between the expression of Fas/FasL and the apoptosis in retinal ischemia/reperfusion injury of rats, as well as the therapeutic effects of basic fibroblast growth factor (bFGF)on the ischemic retina.injury were made by transiently elevating introcular pressure. A total of 28 rats were divided into Normal Group and Operative Group. The latter were subdivided into 1, 6, 12, 24, 48 and 72h after reperfusion, in which the left eyes of the rats were in the ischemia/reperfusion groups and the right ones were in the treatment groups (bFGF intracameral injection). Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) method, and theexpression of Fas/FasL ligand was studied by strept avidin-biotin complex (SABC) immunohistochemistry.mai rats' retinae, but there were a significant number of TUNEL positive cells in 6-24h after transient ischemia followed by a decrease at 48h. The number of TUNEL positive cells reached a maximum at 24h after ischemia.The expression of Fas gradually increased as early as at 6h, reached a peak at 24h, then decreased at 48h. Similarly, the expression of Fas ligand was at peak in 24-48h in GCL and INL of retina. bFGF ministered before reperfusion inhibited apoptotsis and ameliorated the tissue damage. It also diminished Fas and FasL expression in ischemic/reperfused retina.siently elevated IOP induced apoptosis of cells in the retina. Fas/FasL may have an important role in the early events of the apoptotic pathways. bFGF can rescue RGCs from retinal ischemia/reperfusion injury through down-regulation of Fas and Fas ligand expression and may represent an important mechanism for therapeutic neuroprotection.
