Chen Guo-ling, Liu Zhi-yu, Wang Jing, Gao Xue, Wei Lu-wan, Liu Yan-li
Ophthalmic Center/Department of Ophthalmology, Second Hospital, Shandong University, Jinan 250033, China.
Chin Med Sci J. 2009 Dec;24(4):236-40. doi: 10.1016/s1001-9294(10)60008-9.
To investigate the effect of emodin on lipopolysaccharides (LPS)-induced corneal injury in rats.
Three parallel incisions on the central surface of corneal epithelium were made and LPS was applied on them to induce corneal injury in Wistar rats. All rats were randomly divided into emodin group (n=40) and keratitis group (n=40). Rats in the emodin group received subconjunctival injection of emodin and rats in the keratitis group received its vehicle 30 minutes before LPS exposure. At different time points--1, 3, 6, 12, and 24 hours after LPS exposure, the symptoms of all rats were observed and the severity of their ocular inflammation was examined with a slit lamp microscope, then 8 rats in each group were killed through cervical dislocation and their eyes were enucleated and prepared to observe pathological changes of corneal tissue under a light microscope. The activation of nuclear factor-kappaB (NF-kappaB) under different conditions was determined by Western blot. Immunocytochemistry staining with an antibody against intercellular adhesion molecule-1 (ICAM-1) was performed to identify positive cells in corneal tissues.
The model of acute keratitis was successfully established in Wistar rats. LPS could induce a typical corneal inflammatory response, such as hyperemia, corneal edema and opacity, which were observed in model rats. Compared with keratitis group, both ocular behaviors and damages of the corneal structure were improved in emodin group. Furthermore, the activation of NF-kappaB and the expression of ICAM-1 induced by LPS were markedly inhibited in emodin group.
Emodin can inhibit the activation of NF-kappaB and the expression of ICAM-1 induced by LPS in corneas, protect against acute corneal injury, and improve symptoms in rats.
研究大黄素对脂多糖（LPS）诱导的大鼠角膜损伤的影响。
在Wistar大鼠角膜上皮中央表面制作三条平行切口，在切口处应用LPS诱导角膜损伤。所有大鼠随机分为大黄素组（n = 40）和角膜炎组（n = 40）。大黄素组大鼠在暴露于LPS前30分钟接受结膜下注射大黄素，角膜炎组大鼠接受其溶媒。在LPS暴露后的不同时间点——1、3、6、12和24小时，观察所有大鼠的症状，并用裂隙灯显微镜检查其眼部炎症的严重程度，然后每组处死8只大鼠，通过颈椎脱臼法处死，摘除眼球，制备角膜组织，在光学显微镜下观察病理变化。通过蛋白质免疫印迹法测定不同条件下核因子κB（NF-κB）的激活情况。用抗细胞间黏附分子-1（ICAM-1）抗体进行免疫细胞化学染色，以鉴定角膜组织中的阳性细胞。
在Wistar大鼠中成功建立了急性角膜炎模型。LPS可诱导典型的角膜炎症反应，如模型大鼠出现的充血、角膜水肿和混浊。与角膜炎组相比，大黄素组的眼部行为和角膜结构损伤均得到改善。此外，大黄素组中LPS诱导的NF-κB激活和ICAM-1表达明显受到抑制。
大黄素可抑制角膜中LPS诱导的NF-κB激活和ICAM-1表达，预防急性角膜损伤，并改善大鼠症状。
