Guo-Ling Chen1, Jing-Jing Zhang2, Xin Kao1, Lu-Wan Wei3, Zhi-Yu Liu3. 1. Department of Ophthalmology, the Second Hospital of Shandong University, Jinan 250033, Shandong Province, China. 2. Department of Ophthalmology, the Third People's Hospital of Jinan, Jinan 250101, Shandong Province, China. 3. Department of Anatomy, Shandong Univeristy School of Medicine, Jinan 250012, Shandong Province, China.
Abstract
AIM: To investigate the effect of emodin on pseudomonas aeruginosa lipopolysaccharides (LPS)-induced corneal inflammation in rats. METHODS: Corneal infection was induced by pseudomonas aeruginosa LPS in Wistar rats. The inflammation induced by LPS were examined by slit lamp microscope and cytological checkup of aqueous humor. Corneal tissue structure was observed by hematoxylin and eosin (HE) staining. The activation of nuclear factor kappaB (NF-κB) was determined by Western blot. Messenger ribonucleic acid (mRNA) of tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) in LPS-challenged rat corneas were measured with reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Typical manifestations of acute corneal inflammation were observed in LPS-induce rat model, and the corneal inflammatory response and structure were improved in rats pretreated with emodin. Treatment with emodin could improve corneal structure, reduce corneal injure by reducing corneal inflammatory response. Emodin could inhibit the decreasing lever of inhibitor of kappaB alpha (IкBα) express, and the mRNA expression of TNF-α and ICAM-1 in corneal tissues was also inhibited by emodin. The differences were statistically significant between groups treated with emodin and those without treatment (P<0.01). CONCLUSION: Emodin could ameliorate LPS-induced corneal inflammation, which might via inhibiting the activation of NF-κB.
AIM: To investigate the effect of emodin on pseudomonas aeruginosalipopolysaccharides (LPS)-induced corneal inflammation in rats. METHODS:Corneal infection was induced by pseudomonas aeruginosaLPS in Wistar rats. The inflammation induced by LPS were examined by slit lamp microscope and cytological checkup of aqueous humor. Corneal tissue structure was observed by hematoxylin and eosin (HE) staining. The activation of nuclear factor kappaB (NF-κB) was determined by Western blot. Messenger ribonucleic acid (mRNA) of tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) in LPS-challenged rat corneas were measured with reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Typical manifestations of acute corneal inflammation were observed in LPS-induce rat model, and the corneal inflammatory response and structure were improved in rats pretreated with emodin. Treatment with emodin could improve corneal structure, reduce corneal injure by reducing corneal inflammatory response. Emodin could inhibit the decreasing lever of inhibitor of kappaB alpha (IкBα) express, and the mRNA expression of TNF-α and ICAM-1 in corneal tissues was also inhibited by emodin. The differences were statistically significant between groups treated with emodin and those without treatment (P<0.01). CONCLUSION: Emodin could ameliorate LPS-induced corneal inflammation, which might via inhibiting the activation of NF-κB.
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