Departmnet of Ophthalmology, Beijing Chaoyang Hospital, Capital Medical University, No. 8 Baijiazhuang Road, Chaoyang District, Beijing 100020, China.
Mediators Inflamm. 2010;2010:748218. doi: 10.1155/2010/748218. Epub 2010 Aug 3.
To observe the expression of Toll-like receptor-4 (TLR4), myeloid differentiation factor 88 (MyD88), and nuclear factor kappa B p65 (NF-κB p65) in iris tissue during endotoxin-induced uveitis (EIU) and evaluate the significance of these factors in uveitis.
Wistar rats were randomly divided into 5 groups (0 h, 12 h, 24 h, 48 h, and 72 h, n = 10/group). Animal model of acute anterior uveitis was established by a hind footpad injection of 200 μg Cholera vibrio LPS. Expression of TLR4, MyD88, and NF-κB p65 in iris ciliary body tissue was detected through immunohistochemical staining.
Expression of TLR4 was not detected in normal iris-ciliary body complex, TLR4 positive cells with round morphology appeared in the iris stroma 12 hours after injection, significantly increased (P < .001) 48 hours after injection, and decreased gradually 72 hours after injection. Expression of MyD88 and NF-κB p65 is consistent with the change of the TLR4.
The increased expression of TLR4 and its downstream signal transduction moleculesMyD88, NF-κB p65 indicate the potential role of pathway in the pathogenesis of acute anterior uveitis (AAU).
观察脂多糖诱导的葡萄膜炎（EIU）模型中虹膜组织中 Toll 样受体 4（TLR4）、髓样分化因子 88（MyD88）和核因子 kappa B p65（NF-κB p65）的表达，评估这些因子在葡萄膜炎发病机制中的意义。
Wistar 大鼠随机分为 5 组（0 h、12 h、24 h、48 h 和 72 h，每组 n = 10）。通过后足底注射 200 μg霍乱弧菌 LPS 建立急性前葡萄膜炎动物模型。采用免疫组织化学染色法检测虹膜睫状体组织中 TLR4、MyD88 和 NF-κB p65 的表达。
正常虹膜睫状体复合体中未检测到 TLR4 表达，注射后 12 小时虹膜基质中出现圆形形态的 TLR4 阳性细胞，明显增加（P <.001），48 小时后逐渐减少，72 小时后注射后逐渐减少。MyD88 和 NF-κB p65 的表达与 TLR4 的变化一致。
TLR4 及其下游信号转导分子 MyD88、NF-κB p65 的表达增加表明该途径在急性前葡萄膜炎（AAU）发病机制中的潜在作用。
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