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

BACKGROUND

Gastric ulcer (GU) is one of the most critical gastrointestinal tract disorders. Garcinol is a polyisoprenylated benzophenone in Garcinia fruit with antioxidant and anti-inflammatory priorities.

OBJECTIVES

We aimed to assess the protective effects of garcinol against GU induced in rats. We investigated garcinol's effects on DNA polymerization via mammalian targets of rapamycin (mTOR) and cyclin D1, cell proliferation via proliferating cell nuclear antigen (PCNA), inflammatory pathway via cyclooxygenase-2 (COX2), TNF-α, and IL-1β, and anti-inflammatory pathway via IL-4 and IL10.

METHODS

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.

RESULTS

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 in gastric 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.

CONCLUSION

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.