Abstract
This study investigated the therapeutic role of polysaccharides from M. charantia and their mechanism of action against ethanol-induced gastric ulcers in rats. Their effects were determined through macroscopic evaluation of the gastric cavity (gastric ulcer index [GUM, changes in PGE(2), lipid peroxidation (malondialdehyde), antioxidant systems (catalase and reduced glutathione), inflammatory markers (tumor necrosis factor-alpha [TNF-alpha], interleukin-6 (IL-6], and myeloperoxidase (MPO]), apoptotic markers (caspase 3, Bax, and BcI-2), nuclear factor-KB (NF-KB [p65]), and histopathological staining (H&E and PAS). Pretreatment with MCP (300 mg/kg p. o.) attenuated the severity of ethanol-induced gastric mucosal damage, reductions in GUI, histopathologic aberrations, and neutrophil invasion, and PGE(2) upregulation. These actions were similar to those of omeprazole, a reference anti-ulcer drug. MCP repressed gastric inflammation through the reduction of MPO, TNF-a, and IL-6, and prevented gastric oxidative stress through the inhibition of lipid peroxides with the concomitant enhancement of glutathione and catalase activity. Apoptotic markers indicated that MCP suppressed Bax and caspase-3 activity and enhanced the anti-apoptotic protein Bcl-2, which favored cell survival. MCP downregulated NF-KB and up regulated IKB alpha. Our study results suggested that the prophylactic administration of MCP reduced ethanol induced gastric injury in rats through the suppression of gastric inflammation and oxidative stress, predominantly via NF-KB inhibition. (C) 2018 Elsevier B.V. All rights reserved.