摘要
目的:观察角膜炎大鼠动物模型的组织特征和眼部表现,探讨细胞间粘附分子(intercellularadhesion molecule,ICAM)-1在绿脓杆菌脂多糖(lipopolysaccharide,LPS)诱导的急性角膜炎大鼠角膜组织中的表达及意义。方法:角膜炎动物模型制作前30 min,分别在大鼠球结膜下注射二硫代氨基甲酸吡咯烷(pyrrolidine dithiocarbamate,PDTC)(PDTC预处理组)和生理盐水(炎症组)。LPS刺激后1、3、6、12、24 h时,用裂隙灯显微镜观察大鼠的眼部表现并评分;抽取大鼠房水立即涂片,光镜观察房水细胞变化;透射电子显微镜观察角膜组织超微结构的改变。免疫组织化学法检测角膜组织内ICAM-1蛋白的表达。结果:预先用PDTC处理后再给予LPS刺激,可明显改善大鼠角膜炎症状、减轻角膜及房水混浊的程度。PDTC预处理组大鼠房水的细胞改变及角膜的超微结构变化较炎症组均有明显改善,角膜组织中ICAM-1的表达在各个时段较炎症组均有不同程度的降低(P<0.01)。结论:绿脓杆菌LPS参与了大鼠急性角膜炎的病理过程;PDTC可下调角膜组织ICAM-1的表达,有效减轻了LPS引起的角膜炎症。
Objective: To investigate the clinical representation and tissue feature of acute keratitis in the rat model, and to investigate the expression and significance of intercellular adhesion molecule(ICAM)-1 in corneas of lipopolysaccharide(LPS)-induced keratitis rats. Methods: Thirty minutes before the keratitis was induced by LPS, PDTC and saline were injected into the sub-conjunctiva of the Wistar rats, respectively, then 1,3,6,12 and 24 hours after LPS exposure, the opacity of cornea and aqueous humor was observed by slit-lamp microscope, and the aqueous humor was detected by histological analysis. Corneal ultra-structural morphology was observed by transmission electron microscope (TEM). Expression of ICAM-1 was detected by immunohistochemical staining. Results: Both symptoms and damages of cornea were slighter in the PDTC pretreated group than those in the keratitis group. Compared with the rats treated with normal saline, the expression of ICAM-1 was significantly down-regulated after LPS challenge from 1 hour to 24 hours in PDTC Dretreated group (P 〈0.01, seoaratively). Conclusion: LPS takes part in the pathogenesis of experimental keratitis in rats. PDTC can inhibit the release of ICAM-1 and alleviate the acute injury in rats cornea.
出处
《山东大学学报(医学版)》
CAS
北大核心
2006年第4期429-432,共4页
Journal of Shandong University:Health Sciences
基金
国家自然科学基金资助课题(0328026)