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Establishing a Severe Corneal Inflammation Model in Rats Based on Corneal Epithelium Curettage Combined with Corneal Sutures
Published on: November 22, 2024
Emodin ameliorates lipopolysaccharides-induced corneal inflammation in rats
Guo-Ling Chen1, Jing-Jing Zhang2, Xin Kao1
1Department of Ophthalmology, the Second Hospital of Shandong University, Jinan 250033, Shandong Province, China.
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.
Insights
Emodin effectively reduced inflammation and improved corneal structure in a rat model of Pseudomonas aeruginosa lipopolysaccharide-induced keratitis. This suggests emodin may inhibit nuclear factor-kappaB (NF-κB) activation.
Area of Science:
- Ophthalmology
- Pharmacology
- Immunology
Background:
- Corneal inflammation is a significant cause of vision impairment.
- Bacterial lipopolysaccharides (LPS) are potent inducers of ocular inflammation.
- Nuclear factor-kappaB (NF-κB) signaling plays a critical role in inflammatory processes.
Purpose of the Study:
- To evaluate the therapeutic potential of emodin in a rat model of Pseudomonas aeruginosa LPS-induced corneal inflammation.
- To investigate the underlying molecular mechanisms of emodin's anti-inflammatory effects in the cornea.
Main Methods:
- Corneal inflammation was induced in Wistar rats using Pseudomonas aeruginosa LPS.
- Ocular inflammation was assessed via slit lamp microscopy and aqueous humor cytology.
- Corneal tissue structure was analyzed using hematoxylin and eosin (HE) staining.
- NF-κB activation, IκBα degradation, and mRNA expression of TNF-α and ICAM-1 were quantified using Western blot and RT-PCR.
Main Results:
- LPS challenge induced typical signs of acute corneal inflammation.
- Emodin pretreatment significantly ameliorated corneal inflammation and improved corneal tissue structure.
- Emodin inhibited the degradation of IκBα and reduced the mRNA expression of TNF-α and ICAM-1.
- Statistical analysis confirmed significant differences between emodin-treated and untreated groups (P<0.01).
Conclusions:
- Emodin demonstrates significant therapeutic efficacy in mitigating LPS-induced corneal inflammation in rats.
- The anti-inflammatory effects of emodin may be attributed to the inhibition of NF-κB activation.
- Emodin holds promise as a potential treatment for bacterial keratitis.
