Gastric healing effect ofp-coumaric acid isolated fromBaccharis dracunculifoliaDC on animal model

Thep-coumaric acid is a phenolic compound present in large quantities in the extract ofBaccharis dracunculifoliaDC, a Brazilian medicinal plant used to treat gastric ulcer. Given the necessity for finding new chemical components capable of accelerating gastric healing, in this study, the effects of thep-coumaric acid were evaluated in the acetic acid-induced ulcer model in rats, where histological, inflammatory, and oxidative parameters were analyzed. The healing property was also evaluated in the scratch assay on fibroblast cells (L929) and the cytotoxicity ofp-coumaric acid was assessed in both L929 and human gastric adenocarcinoma (AGS) cells by MTT assay. The treatment withp-coumaric acid (10 mg/kg, p.o.) for 7 days, twice a day, decreased by 44.6% the acetic acid-induced gastric ulcer compared with the vehicle-treated group. The vehicle control-treated group showed a larger extension of the ulcer base and an extensive damage into the mucosa and submucosa layers, which were mitigated by the treatment withp-coumaric acid. This beneficial effect was also associated with increased levels of mucin and reduced glutathione, decreased amount of lipid hydroperoxides, and increased superoxide dismutase and catalase activities without interfering with the activity of myeloperoxidase in the gastric tissue. The compound promoted the restructuring of the cell monolayer in the scratch test and did not show toxicity in the L929 cell line, while reduced the viability of the AGS, a lineage of human gastric adenocarcinoma. Thus,p-coumaric acid may be considered a natural source for the treatment of gastric ulcers, by reinforcing protective factors of gastric mucosa and by accelerating gastric healing.

Automated summary

p-Coumaric acid showed beneficial effects in reducing acetic acid-induced gastric ulcer by increasing mucin and reduced glutathione levels, decreasing lipid hydroperoxides, and increasing superoxide dismutase and catalase activities. It also accelerated cell monolayer restructuring during healing process without toxicity to fibroblast cells, but reduced viability in human gastric adenocarcinoma cells.