lnfluence of dexamethasone on lL-1β and TNF - α expression in rabbit corneal neovascularization
10.3980/j.issn.1672-5123.2014.09.04
- VernacularTitle:地塞米松对兔角膜新生血管组织中 lL-1β及 TNF-α表达的影响
- Author:
Rui, SHI
;
Yu-Shun, XUE
;
Le, YANG
;
Ji-Min, WANG
;
Feng, WANG
;
Yi-Ning, SHI
- Publication Type:Journal Article
- Keywords:
corneal neovascularization;
interleukin - 1β;
tumor necrosis factor-α;
inflammatory;
dexamethasone
- From:
International Eye Science
2014;(9):1574-1577
- CountryChina
- Language:Chinese
-
Abstract:
To discuss the influence of dexamethasion on lL-1β and TNF - α expression in suture - induced rabbit corneal neovascularization ( CNV ) and analyze the potential mechanism.
●METHODS: For 43 healthy rabbits, 40 were randomly selected for establishing CNV model in corneal stroma. The right eyes (group A) were received no medicine and the left eyes ( group B) were injected dexamethasone after successfully establishing the model. The no modeling 3 rabbits were normal control group. The morphologic change of corneal was observed with slit lamp microscope and the areas of CNV was calculated every day, then 8 rabbits were randomly chosen for sacrificing at 1, 4, 7, 14, 21d respectively. The pathological characteristics of CNV were observed after HE staining, and lL - 1β and TNF - α expression was detected by immunohistochemistry.
●RESULTS: CNV was grown at the 4d after suture, and the 7-14d was vigorous growth period. inflammatory cell infiltration appeared after HE staining, and CNV was located at the superficial stroma of cornea. lmmunohistochemistry results showed that lL - 1β and TNF - α expression was gradually increased with prolonged suture time. Compared with corneal stitch group, the rabbits cured by dexamethasone were found with less inflammatory cells infiltrating and neovescularization, moreover, the expression of lL - 1βand TNF-α decreased. There were statistical significance between the two groups (P<0. 05).
● CONCLUSlON: Dexamethasone can inhibit the CNV growth by controlling the inflammation of corneal and restraining lL-1β and TNF-α expression.
