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目的观察内毒素诱导的大鼠急性前葡萄膜炎(EIU)虹膜组织内Toll样受体4(TLR4)、髓样分化因子88(MyD88)及核因子-κBp65(NF-κB p65)的表达。方法Wistar大鼠50只,随机分为5组,0、12、24、48、72h,每组10只,0h组为正常对照组,其余4组均足垫部注射霍乱弧菌内毒素脂多糖(LPS)200μg,建立EIU动物模型,每隔2h用裂隙灯观察大鼠眼前节炎症反应。通过铺片免疫组织化学染色,检测虹膜睫状体组织内TLR4、MyD88和NF-κBp65的表达,并对虹膜内TLR4+和MyD88+及NF-κBp65+细胞进行计数。结果注射后24～48h大鼠眼前段的炎症反应达到高峰,72h炎症反应逐渐缓解。组织病理学检查表明,虹膜睫状体组织的炎性细胞浸润在24～48h达到高峰,与临床反应结果相符。TLR4在模型鼠虹膜睫状体炎复合体中表达的免疫组织化学检测结果表明,0h组虹膜铺片内无阳性细胞,12h后可见细胞形态大多为类圆形的阳性细胞,48h达高峰,72h阳性细胞数开始减少,各组阳性细胞数总体差异有统计学意义(F=46.79,P<0.05)。MyD88和NF-κBp65的表达与TLR4的改变趋势相一致(F=54.37,P<0.05;F=85.32,P<0.05)。结论内毒素诱导的EIU虹膜内,TLR4及其下游信号传导分子的表达量发生改变,提示TLR4-MyD88依赖传导途径可能参与了EIU的发病。
Objective To observe the expression of TLR4, MyD88 and NF-κB p65 in endotoxin-induced iris in rats with acute anterior uveitis (EIU). Methods Fifty Wistar rats were randomly divided into five groups: 0,12,24,48 and 72h, each group had 10 rats. The rats in 0h group were normal control group. The other 4 groups were injected with V. cholerae lipopolysaccharide (LPS) 200μg, established animal model of EIU, slit lamp observation every 2h inflammation of the anterior segment of the rat. The expression of TLR4, MyD88 and NF-κBp65 in iris and ciliary body tissues were detected by immunohistochemical staining. The numbers of TLR4 +, MyD88 + and NF-κBp65 + in the iris were counted. Results Inflammatory reaction in the anterior segment of the anterior chamber reached a peak at 24-48 hours after injection, and the inflammatory response was gradually relieved at 72 hours. Histopathological examination showed that inflammatory cell infiltration in the iris ciliary body peaked at 24-48 h, consistent with the clinical response. Immunohistochemical results of TLR4 expression in the model rat iridocyclitis complex showed that there was no positive cells in 0h group iris patch. After 12h, most of the cells were round-shaped cells, reaching the peak at 48h, 72h The number of positive cells began to decrease, and there was a significant difference in the number of positive cells in each group (F = 46.79, P <0.05). MyD88 and NF-κBp65 expression consistent with the trend of TLR4 changes (F = 54.37, P <0.05; F = 85.32, P <0.05). Conclusion The expression of TLR4 and its downstream signaling molecules in endotoxin-induced EIU iris changes, suggesting TLR4-MyD88-dependent pathway may be involved in the pathogenesis of EIU.