Effects of emodin on expression of cytokines induced by lipopolysaccharide in corneal fibroblasts / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate the effects of emodin on expression of cytokines induced by lipopolysaccharide (LPS) in cultured human corneal fibroblasts in vitro.</p><p><b>METHODS</b>Primary human corneal fibroblasts of passages 4 were used in this research. Cells were treated with 10 microg/L LPS for 1, 2, 4, or 8 hours, which were pretreated with or without emodin for 30 minutes before LPS challenge. The degeneration of inhibitor of kappaB-alpha (I kappaB-alpha) and the effect of emodin on it were analyzed by Western blot analysis with a specific antibody. The cellular abundance of the mRNA of interleukin (IL)-6 and IL-8 from corneal fibroblasts under different conditions was determined by reverse transcriptase polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>Compared with cells without LPS treatment, I kappaB-alpha level significantly decreased in every time point after LPS challenge (P < 0.01). Emodin inhibited the LPS-induced degeneration of I kappaB-alpha by corneal fibroblasts in a dose-dependent manner (P < 0.05). Compared with cells without LPS treatment, the expressions of IL-6 and IL-8 mRNA significantly increased in every time point after LPS challenge (P < 0.01). At the same time, the expressions of the mRNA of IL-6 and IL-8 induced by LPS in corneal fibroblasts were also inhibited by emodin in a dose-dependent manner (P < 0.05).</p><p><b>CONCLUSION</b>Emodin can inhibit the expressions of IL-6 and IL-8 mRNA induced by LPS in corneal fibroblasts, which maybe via inhibiting the degeneration of I kappaB-alpha and suppressing the activation of nuclear factor-kappaB.</p>

Protective effect of emodin against lipopolysaccharides-induced corneal injury in rats / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effect of emodin on lipopolysaccharides (LPS)-induced corneal injury in rats.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>