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The Improvement of Experimentally Induced Gastric Ulcers in Rats by Inhibiting Vascularization Through the Blocking
Abdullah Alattar1, Reem Alshaman1, Fawaz E Alanazi1
1Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Tabuk, Tabuk, Saudi Arabia.
Background:
About 5%-10% of the world's population is affected by gastric ulcers, which can result in gastrointestinal perforation and bleeding. Consequently, we aimed to investigate whether blocking TNF-α type 1 receptor (TNFR1) with CAY10500 could diminish experimentally induced gastric ulcer (GU) in rats by modulating vascularization.
Methods:
Rats were administered with a single oral dose of 80 mg/kg of indomethacin to produce gastric ulcers. Subsequently, some rats were given 1 mg/kg of CAY10500 orally. Gastric samples were used to assess the genetic expression and protein levels of TNFR1, VEGF, ERK, PI3K, AKT (also known as PKB), and ICAM-1. Gastric sections underwent electron microscopic examination and were subjected to hematoxylin and eosin staining and immunostaining using anti-TNFR1, anti-VEGF, and anti-ICAM-1 antibodies.
Results:
CAY10500 demonstrated the ability to inhibit the expression of TNFR1. Examination of micro-images of GU using electron microscopy or H/E staining revealed extensive necrosis, resulting in the complete loss of regular ultrastructural features of epithelial nuclei and cytoplasmic organelles, as well as the loss of tight junctions and disruption of cell membranes. Significantly, the administration of CAY10500 mitigated these effects. Furthermore, CAY10500 significantly elevated the expressions of VEGF, ERK, PI3K, and AKT, which was associated with a significant reduction in the expression of ICAM-1.
Conclusion:
CAY10500 effectively improved experimentally induced GU in rats. It works by inhibiting TNFR1 and activating angiogenesis and cell proliferation pathways, leading to gastric tissue healing. CAY10500 significantly reduced the adhesion molecule pathways.
Insights
CAY10500 treatment significantly reduced gastric ulcers in rats by blocking TNF-alpha type 1 receptor (TNFR1). This action promoted healing through enhanced vascularization and cell proliferation, while reducing inflammation.
Area of Science:
- Gastroenterology
- Pharmacology
- Molecular Biology
Background:
- Gastric ulcers affect 5%-10% of the global population, leading to severe complications like perforation and bleeding.
- Investigating novel therapeutic targets for gastric ulcer treatment is crucial.
Purpose of the Study:
- To evaluate the efficacy of CAY10500, a tumor necrosis factor-alpha type 1 receptor (TNFR1) inhibitor, in mitigating experimentally induced gastric ulcers in rats.
- To explore the underlying mechanisms of CAY10500, focusing on vascularization and cellular pathways.
Main Methods:
- Gastric ulcers were induced in rats using indomethacin.
- Rats were treated with CAY10500, and gastric tissues were analyzed for gene and protein expression of TNFR1, VEGF, ERK, PI3K, AKT, and ICAM-1.
- Histopathological and ultrastructural analyses were performed using electron microscopy, H/E staining, and immunostaining.
Main Results:
- CAY10500 effectively inhibited TNFR1 expression and mitigated gastric ulcer-induced tissue damage, including necrosis and loss of cellular integrity.
- Treatment with CAY10500 significantly increased the expression of vascular endothelial growth factor (VEGF), ERK, PI3K, and AKT.
- CAY10500 administration led to a significant decrease in intercellular adhesion molecule-1 (ICAM-1) expression.
Conclusions:
- CAY10500 demonstrates significant therapeutic potential for treating gastric ulcers by inhibiting TNFR1.
- The drug promotes gastric tissue healing via activation of angiogenesis and cell proliferation pathways.
- CAY10500 effectively reduces inflammatory pathways mediated by adhesion molecules.
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