Effects and mechanism of peroxiredoxin-6 on uItravioIet induced corneaI injury in rats
10.11665/j.issn.1000-5048.20160112
- VernacularTitle:过氧化物酶6对紫外线致大鼠角膜损伤的治疗作用及机制
- Author:
Jiahui LYU
;
Minmin JIANG
;
Hui SHI
;
Jianyuan LI
;
Zhenning DU
- Publication Type:Journal Article
- Keywords:
peroxiredoxin-6;
ultraviolet;
cornea;
p38 MAPK;
antioxidation;
injury
- From:
Journal of China Pharmaceutical University
2016;(1):84-89
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the therapeutic effect of peroxiredoxin-6(PRDX6)on ultraviolet-induced corneal injury in rats and explore the mechanism.The rat model of corneal injury was established by exposing to ultravio-let.Male wister rats were randomly divided into control groups,dexamethasone (DXM)groups and PRDX6 groups,the rats were administered four times a day and for 12 days.The corneal opacity was observed with a slit-lamp microscope.Histopathologic changes were observed with light microscopy.The content of corneal malonalde-hyde(MDA)was determined by thiobarbituric acid test and the total antioxidative capacity(TAOC)was detected by chemical colorimetric test.P38 MAPK signal pathway was detected with the method of Western blot and the gene expression of cytokines were measured by RT-PCR method.Compared with the control group,PRDX6 treat-ment significantly reduced corneal opacity,improved corneal pathology injury,decreased the MDA content and in-creased the TAOC.In the PRDX6 group the level of phosphorylated p38 protein was significantly lower than that in the control group.The gene expression of cytokine were different between control and PRDX6 groups(P <0.05).PRDX6 showed therapeutic effect in the rat model of ultraviolet-induced corneal injury.This maybe be concerned with that it could alleviated the oxidative damage,suppressed p38 MAPK phosphorylation and regulate the gene expression of cytokine.
