中文摘要：

背景原子 factor-kappa B (NF-κ B ) 在调整许多 cytokines 和煽动性的调停人的抄写被提高。这研究的目的是调查激活，在脂肪的多糖(LPS ) 的意义 NF-κ B 导致了角膜炎。方法 LPS 导致了角膜炎模型基于 Wistar 老鼠。在 0 点。5， 1， 3， 6， 12，在 LPS 处理以后的 24 个 or72 小时，老鼠角膜与一台裂缝灯显微镜被观察，然后， ther ats 被牺牲，他们的角膜为平淡的组织学的分析被切除。NF-κ B 的 Theexpression 与免疫被检测组织化学的染色。瘤 necrosisfactors- α的变化(TNF- α) mRNA 表示被反向的 transcriptase 聚合酶链反应(RT-PCR ) 识别。组织学的调查结果表明了的结果 LPS 对待角膜，这在角膜的结构显示出重要变化。角膜的浮肿，显著煽动性的房间渗入和过度的骨胶原纤维被观察。Immunohistochemical 结果证明 NF-κ B 和它的激活的表示显然与正常的组和控制组相比在 LPS 处理以后增加了。积极房间能在 0 点被观察。NF-κ B 的 5 小时和山峰表示在感染以后在 3 个小时和 12 个小时之间被观察，但是回到了或接近了正常水平 by72 小时。RT-PCR 证明 TNF- α mRNA 的水平开始增加了 0。在 LPStreatment 以后的 5 小时，在 6 个小时达到顶点然后到 72 个小时减退了。NF-κ B 与 TNF- α mRNA 的表示有积极关联(r = 0。964， P < 0。01 ) ， NF-κ B 和 TNF- α在 LPS 与煽动性的反应的度有强壮的积极关联对待的角膜(r =0。929， P < 0。01；r=0。587， P < 0。05，分别地) 。NF-κ B 的激活是增加的 inLPS 的结论对待角膜并且在 LPS 被提高由在 TNF-α m RNA 的表示上支持的导致的角膜炎。NF-κ B 可以在老鼠在联系 LPS 的角膜炎的致病起一个重要作用。

英文摘要：

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 ker