Alpha-Mangostin Provides Protection from Mucosal Damage via Prostaglandin E2 in Indomethacin and Ethanol-Induced Gastric Ulcers

Abstract

Objective: Gastric ulcer is frequently observed among the gastrointestinal diseases and is induced by various factors. Alpha-mangostin (α-MG) has antioxidant and anti-inflammatory properties and may prevent gastric ulcers. This study was conducted to evaluate the healing effect of α-MG against gastric ulcer caused by indomethacin (Ind) and ethanol (Eth) in rats. Methods: Wistar albino male rats were used to establish the experimental model. Seven groups were formed, as group I sham, group II (5 mL/kg Eth), group III (100 mg/kg Ind), group IV (Eth + Lansoprazole (Lans) 30 mg/kg), group V (Ind + Lans 30 mg/kg), group VI (Eth + α-MG 10 mg/kg), and group VII (Ind + α-MG 10 mg/kg) (n=10). Cytokines; VEGF-A; NOS2/iNOS; PGE2 levels were analyzed by the ELISA method. Besides, the general appearance of the gastric tissues was evaluated by hematoxylin-eosin staining, COX-1, COX-2, NF-κB, and caspase-3 levels were measured immunohistochemical (IHC). Results: Cytokine levels decreased in the treatment groups compared to the ulcer groups. There was a decrease in VEGF-A and NOS2/iNOS levels in the α-MG administered groups. The reduction in PGE2 levels in the gastric ulcer groups was counteracted by an increase in both the Lans and α-MG administered groups. In the IHC results, while COX-1, COX-2, NF-κB, and caspase-3 levels were increased in gastric ulcer groups, significant decreases were observed in Lans and α-MG groups. Conclusion: As a result, α-MG eased inflammation and increased PGE2 levels. It reduced the levels of COX-1, COX-2, NF-κB, and caspase-3. As a result of these data, α-MG may be a potential therapeutic agent against gastric ulcer.