Therapeutic potential of Ferula foetida(Bunge) Regel on gastric ulcer model in rats

The plant Ferula foetida(Bunge) Regel (FFBR) has a long history in Asian traditional medicine. This study aimed to evaluate the ulcer healing potential of FFBR umbel ethanolic extract on acetic acid-induced chronic gastric ulcer in rats. First, the gastric ulcer model was imitated by serosal application of acetic acid in male Wistar rats. Then, the animals were orally fed by ethanolic extract of FFBR umbel (100 mg/kg, 200 mg/kg, and 300 mg/kg), omeprazole (40 mg/kg), or saline for 12 days. Eventually, on the 13th day, animals were sacrificed, and their stomachs were taken out. The macroscopic and microscopic appearances of gastric ulcers and the levels of malondialdehyde (MDA), vascular endothelial growth factor (VEGF), and prostaglandin E-2 (PGE(2)) in gastric tissues were assessed. In addition, the expression of NF-kappa B p65 was investigated by immunohistochemistry. Compared to the untreated rats with gastric ulcer, FFBR extract significantly decreased ulcer area even superior to omeprazole in a dose-dependent manner. Moreover, histological examination revealed that the extract (300 mg/kg) accelerated the epithelialization and differentiation of proliferative cells to mucosal tissue. The FFBR extract (300 mg/kg) increased tissue levels of VEGF and PGE(2), but it did not affect MDA levels in rats with gastric ulcers. FFBR treatment (all doses) could significantly inhibit the expression of NF-kappa B p65 in gastric tissue. Taken together, experimental findings suggested that FFBR could accelerate the healing process of gastric ulcers in rats through mediating NF-kappa B and VEGF/PGE(2) pathways.

Automated summary

The study demonstrated that the ethanolic extract of Ferula foetida (Bunge) Regel umbel has potential in promoting healing of gastric ulcers in rats by mediating NF-kappa B and VEGF/PGE(2) pathways. This was evidenced by a reduction in ulcer area, accelerated epithelialization, increased levels of VEGF and PGE(2) in tissues, and inhibition of NF-kappa B p65 expression.