The role of NF-kB activation in lipopolysacchavide induced keratitis in rats

Background Nuclear factor-kappa B （NF-kB） is elevated in regulating transcription of many cytokines and inflammatory mediators. The purpose of this study was to investigate the activation and the significance NF-KB in lipopolysaccharide （LPS） induced keratitis. Methods LPS induced keratitis model was based on Wistar rats. At 0. 5, 1, 3, 6, 12, 24 or 72 hours after LPS treatment, the rat corneas were observed with a slit lamp microscope, then the rats were sacrificed and their corneas were excised for routine histological analysis. The expression of NF-kB was detected with immunohistochemical staining. The change identified by reverse transcriptase polymerase of tumour necrosis factors-α （TNF-α） mRNA expression was chain reaction （RT-PCR）. Results Histological findings demonstrated that LPS treated corneas showed significant changes in corneal structure. Corneal edema, pronounced inflammatory cells infiltration and inordinate collagen fibres were observed. Immunohistochemical results showed that the expression of NF-kB and its activation obviously increased after LPS treatment compared with the normal group and control group. Positive cells could be observed at 0. 5 hour and peak expression of NF-kB was observed between 3 hours and 12 hours after infection, but returned to or approached normal level by 72 hours. RT-PCR showed that the level of TNF-α mRNA began to increase 0. 5 hour after LPS treatment, peaked at 6 hours and then subsided by 72 hours. NF-kB had a positive correlation with the expression of TNF-α mRNA （r=0. 964, P 〈 0. 01 ） , both NF-kB and TNF-α had a strong positive correlation with the degree of inflammatory response in LPS treated corneas （ r=0. 929, P 〈 0. 01 ; r=0. 587, P 〈 0.05, respectively）. Conclusions The activation of NF-kB was increased keratitis by promoting overexpression of TNF-α mRNA. LPS-associated keratitis in rats. in LPS treated corneas and was elevated in LPS induced NF-kB may play an important role in the pathogenesis ofLPS-associated keratitis in rats.