AI Article Synopsis

  • Ramelteon (RML) is a powerful drug that targets melatonin receptors and has antioxidant and anti-inflammatory properties, and this study looks at its effects in a rat model of uveitis induced by endotoxins.
  • Twenty-eight rats were divided into four groups to compare the effects of LPS alone and with RML treatment, with analyses conducted on tissue and genetic changes after inducing uveitis.
  • Results indicated that RML reduced inflammation, reversed harmful changes in certain signaling pathways (HIF-1α, eNOS, VEGF), and improved the overall condition in rats treated with RML.

Article Abstract

Purpose: Ramelteon (RML) is a potent, selective agonist of the high-affinity melatonin receptor 1 and 2 receptors. In addition, RML is known to have antioxidant and anti-inflammatory effects. In this study, we aimed to investigate the effects of RML on HIF-1α, VEGF and e-NOS signaling pathway in a rat model of endotoxin-induced uveitis (EIU).

Methods: Twenty-eight Wistar albino rats were divided into 4 groups as controls, lypopolysaccharide (LPS) group (5 mg/kg i.p.), LPS  +  RML group (5 mg/kg i.p and 8 mg/kg orally, respectively) and RML group (8 mg/kg orally). EIU was induced by a single intraperitoneal LPS injection. Histopathological and genetical analyses were performed.

Results: In histopathological analysis, LPS caused mild anterior uveitis characterized by increased surface area of iris leaflets and ciliary body due to edema, mild to moderate congestion, and inflammatory infiltrate 6 h following the injection. The pathological findings were reduced by RML. Higher inflammation levels seen in LPS group were significantly reduced in LPS  +  RML group. Also, HIF-1 α, eNOS and VEGF expressions increased in LPS and decreased in LPS  +  RML group.

Conclusion: RML treatment reversed the changes in the HIF-1α /eNOS/ VEGF signaling pathway in LPS-induced uveitis in rats, preventing the progression of the damage and showed positive effects.

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http://dx.doi.org/10.1177/11206721221123878DOI Listing

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