Garcinol-Attenuated Gastric Ulcer (GU) Experimentally Induced in Rats Via Affecting Inflammation, Cell Proliferation, and DNA Polymerization.

Abstract

Gastric ulcer (GU) is one of the most critical gastrointestinal tract disorders. Garcinolis a polyisoprenylated benzophenone in Garcinia fruit with antioxidant and anti-inflammatory priorities. We aimed to assess the protective effects of garcinolagainst GU induced in rats. We investigated garcinol'seffects on DNA polymerization via mammalian targets of rapamycin(mTOR) and cyclin D1, cell proliferation viaproliferating cell nuclear antigen (PCNA), inflammatory pathway viacyclooxygenase-2 (COX2), TNF-α, and IL-1β, and anti-inflammatory pathwayvia IL-4 and IL10. In our study, we administered a single oral dose of 80 mg/kg of indomethacin to rats to induce GU. Some of the rats were given a treatment of 50 mg/kg of garcinol. We examined the expressions of mTOR, cyclin D1, PCNA, COX2, TNF-α, and IL-1β/4/10 in the gastric tissues. Furthermore, we stained sections of the gastric tissues with Masson trichrome. The areas of gastric tissues in the GU group showed severe hemorrhage and extensive fibrosis. Treating GU rats with garcinol prevented bleeding and ameliorated the fibrosis caused ingastric cells by GU. Moreover, treatment with garcinol significantly decreased the expression of mTOR, cyclin D1, PCNA, COX2, TNF-α, and IL-1β associated with elevation of IL-4 and IL-10. Garcinol has been found to provide therapeutic benefits in rats with induced GU. These benefits may be due to its ability to decrease the expression of DNA polymerization markers, cell proliferation markers, and inflammatory markers at the gene and protein levels.