摘要
目的观察大黄素对角膜炎大鼠角膜组织核因子-κB(NF-κB)活化表达的影响及意义。方法制备角膜炎动物模型。模型制备前30 min,分别于治疗组和炎症组大鼠结膜下注射大黄素及溶剂。裂隙灯显微镜观察大鼠眼部变化;Western blotting检测评价角膜组织NF-κB活化表达;免疫组织化学法检测角膜组织细胞间黏附分子-1(ICAM-1)蛋白的表达。结果成功制备了角膜炎大鼠模型,大黄素可改善角膜炎大鼠的眼部炎症反应,减少角膜组织炎细胞浸润。治疗组κB抑制蛋白α(IκBα)在脂多糖(LPS)刺激后各时点的表达均高于同时点炎症组表达(P<0.01)。LPS刺激可促进ICAM-1在角膜组织的阳性表达,该作用可被大黄素部分抑制。结论大黄素可部分抑制角膜炎大鼠角膜组织中NF-κB活化,有效减轻角膜炎症的损伤。
Objective To investigate the significance and effect of emodin on the activation of nuclear factor-κB （NF-κB）in corneas of keratitis rats.Methods Pseudomonas aeruginosa lipopolysaccharide （LPS）-induced keratitis models were established in Wistar rats.Before LPS exposure （30 minutes）,emodin and its vehicle were injected into subconjunctival tissues of rats in treatment group and inflammation group.At different time after LPS challenge,rats were examined with slit lamp microscope to observe the severity of ocular inflammation.The expression of inhibitor NF-κBα（IκBα）was determined with Western blotting,and intercellular adhesion molecule-1 （ICAM-1 ）was detected with immunohistochemical staining.Results The rat models of keratitis were successfully established.LPS could induce a severe corneal inflammatory response,which could be improved by emodin.IκBαlevel was significantly decreased after LPS exposure,and the degeneration of IκBαinduced by LPS was markedly inhibited by pretreatment with emodin （P＆lt;0.01）.Furthermore,the positive cells of ICAM-1 staining were significantly decreased in treatment group as compared with inflammation group.Conclusion LPS takes part in the activation of NF-κB in keratitis corne-as,and emodin can partly inhibit this activation and result in therapeutic effect.
出处
《山东大学学报（医学版）》
CAS
北大核心
2014年第9期44-47,共4页
Journal of Shandong University:Health Sciences
基金
山东省教育厅科技计划项目(J08LH59)
