The effect of liraglutide, a GLP-1 analog, on indomethacin-induced gastric ulcers in diabetic rats.

Abstract

Purpose: To investigate the potential pleiotropic effects of liraglutide (LG), a glucagon-like-peptide-1 analog, on gastric ulcer prevention in rats with diabetes induced by streptozotocin (STZ).

Methods: We randomly divided 63 male Wistar rats into seven groups. STZ was administered intraperitoneally (IP) to the animals in the diabetic control (group STZ), diabetic control + indomethacin (INDO) (group STZI), STZ + INDO + omeprazole (group OMP), STZ + INDO + LG (0.2 mg/kg) (group 0.2LG), and STZ + INDO + LG (0.4 mg/kg) group (group 0.4LG). We administered OMP IP to group OMP, 0.2 mg/kg LG to group 0.2LG SC, 0.4 mg/kg LG to group 0.4LG SC, normal saline to non-diabetic control (sham group), group STZ, non-diabetic control + INDO (group KI), and group STZI SC. INDO was administered to the animals in groups KI, STZI, OMP, 0.2LG, and 0.4LG by gavage. Then, the caspase-3, epidermal growth factor (EGF), vascular endothelial growth factor-A (VEGF-A), prostaglandin E2 (PGE2), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), superoxide dismutase-1 (SOD-1), glutathione (GSH), and malondialdehyde (MDA) levels were studied.

Results: LG prevented INDO-induced ulcers and decreased apoptosis in the stomach tissue. It increased the SOD-1, GSH, EGF, VEGF-A, and PGE2 levels, and reduced the MDA, IL-6, and TNF-α levels. The anti-ulcer effect of LG was lower, but close to that of OMP.

Conclusion: The antioxidant, anti-inflammatory, and anti-apoptotic effects of LG, its ability to regulate EGF, VEGF-A, and PGE2 levels, and its capacity to reduce blood glucose levels in diabetic rats may contribute to its anti-ulcer effect.