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目的 :明确在细菌内毒素 (L PS)诱导的角膜基质炎中是否存在转录调节因子 -核因子 NF-κB的活化表达。方法 :青年 Wistar大鼠右眼及左眼分别给予细菌内毒素 L PS (4μg·μ1- 1 )及其溶剂 -灭菌 PBS各 10μl角膜内注射。注射后分别于 1小时、 3小时、6小时、 1天、 3天及 7天处死动物。每只角膜标本分为 2份 ,一份行石蜡切片病理学检查 ,一份行冰冻切片进行免疫组织化学分析。结果 :病理学检查 :L PS注射后 1小时即可见角膜缘血管内有炎症细胞聚集 ,随时间延长 ,中央角膜基质区域炎症细胞浸润明显 ,基质水肿 ,部分基质细胞溶解坏死 ,被巨噬细胞吞噬 ,至第 3～ 7天中周边基质内有新生血管生成 ,基质水肿渐减轻 ,细胞外胶原排列紊乱 ,呈典型的角膜基质炎的病理改变。免疫组化检查 :L PS注射后 1小时即出现 NF- κB阳性细胞 ,表现为部分基质细胞核内染色阳性 ,染色强度以 3小时和 6小时为最强 ,随时间延长逐渐减弱 ,至 7天时几乎无阳性细胞。结论 :核因子 NF-κB在实验性角膜基质炎早期存在活化表达。NF- κB在细胞核内出现 ,可能通过与相应致炎基因的启动子与增强子结合 ,促进相关基因的转录 ,从而在角膜基质炎中起到重要作用
Objective: To determine whether activated transcription factor NF-κB is present in corneal stroma induced by bacterial endotoxin (LPS). Methods: Young Wistar rats were injected intraperitoneally with 10μl of bacterial endotoxin L PS (4μg · μ1-1) and its solvent-sterile PBS respectively. Animals were sacrificed at 1 hour, 3 hours, 6 hours, 1 day, 3 days and 7 days after injection. Each cornea specimen was divided into 2 parts, a paraffin section pathological examination, a line of frozen sections for immunohistochemical analysis. Results: The pathological examination showed that within 1 hour after the injection of LPS, corneal limbal blood vessels showed accumulation of inflammatory cells. Infiltration of inflammatory cells in the corneal stroma area was evident over time. Edema of the cornea and some stromal cells were lysed and necrotic, and phagocytosis by macrophages , To 3 to 7 days in the surrounding matrix neovascularization, stromal edema diminished, extracellular collagen disordered, showing a typical pathological changes of corneal stromal inflammation. Immunohistochemical examination: NF-κB positive cells appeared one hour after LPS injection and showed positive staining in some stromal nuclei. The intensity of staining was strongest at 3 hours and 6 hours, gradually weakened with time, almost to 7 days No positive cells. CONCLUSION: The nuclear factor NF-κB exists in the early stage of experimental corneal inflammation. NF-κB appears in the nucleus, which may play an important role in corneal inflammation by promoting the transcription of related genes by binding with promoters and enhancers of the corresponding inflammatory genes