Protective effect of non-mitogenic haFGF on retinal injury induced by N-methyl-N-nitrosourea in Sprague-Dawley rats.
- Author:
Hua XU
1
;
Jin-nan YANG
;
Qing ZHENG
;
Cheng-can YAO
;
Yan-ping WANG
;
Ji-zhou XIANG
;
Xiao-kun LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Female; Fibroblast Growth Factor 1; genetics; pharmacology; Methylnitrosourea; Photoreceptor Cells, Vertebrate; drug effects; pathology; Protective Agents; pharmacology; Proto-Oncogene Proteins c-bcl-2; metabolism; Random Allocation; Rats; Rats, Sprague-Dawley; Retina; drug effects; pathology; Retinitis Pigmentosa; chemically induced; metabolism; pathology; bcl-2-Associated X Protein; metabolism
- From: Acta Pharmaceutica Sinica 2005;40(4):306-310
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the effect of non-mitogenic human acidic fibroblast growth factor (nm-haFGF) on retinal injury induced by N-methyl-N-nitrosourea (MNU) in Sprague-Dawley rats and its mechanism.
METHODSFemale rats of 50-days-old were injected with MNU (60 mg x kg(-1)) intraperitoneally, and three doses of nm-haFGF (1.25 microg, 2.5 microg and 5 microg in one eye of each rat) were injected, separately, into vitreous body of one eye of each rat twice a day at 0 and 12 h after MNU treatment. 24 h later, apoptotic index of photoreceptor cells was detected by TUNEL labeling and the expressions of Bcl-2 and Bax were analyzed by Western blotting. At the 7th day, retinal injury was evaluated based on retinal thickness.
RESULTSCompared with model group, apoptotic index of photoreceptor cells was significantly reduced in nm-haFGF groups at the dose of 1.25 microg and 2.5 microg in one eye of each rat at 24 h, and the total retinal thickness as well as the outer retinal thickness markedly increased 7 days after MNU, respectively. The expressions of Bcl-2 increased and that of Bax decreased adversely after being injected with different doses of nm-haFGF.
CONCLUSIONnm-haFGF partially suppressed retinal injury induced by MNU in Sprague-Dawley rats. The mechanism could be related to up-regulation of Bcl-2 and down-regulation of Bax.