Alterations of matrix metalloproteinases, gastric mucin and prostaglandin E(2) levels by pectic polysaccharide of swallow root (Decalepis hamiltonii) during ulcer healing.

Gastric ulcer is a multi-step disease caused due to imbalance between mucosal defense and aggressive factors. Available anti-ulcer drugs although effective at various steps of ulcer pathogenecity, pose adverse effects. Pectic polysaccharide (SRPP) from swallow root (Decalepis hamiltonii) - previously shown to possess ulcer preventive effect against swim stress and ethanol induced gastric ulcers. In the current study, alteration of matrix metalloproteinases, gastric mucin and prostaglandin E(2) levels during polysaccharide mediated ulcer healing was determined in acetic acid induced gastric ulcer model in Wistar albino rats. Results indicated the potential ulcer healing effect of SRPP as evidenced by approximately 90% reduction in ulcer index; improvement in the antioxidant defense such as increase of glutathione levels together with significant reduction in lipid and protein oxidation and protection to damaged gastric mucin. Further, histological studies substantiated the result of the recovery of mucin that was eroded during ulceration, rejuvenation of mucosal epithelium and enhancement of high molecular mass mucin as opposed to the degraded approximately 55 kDa mucin that appeared only during ulcer condition. Matrix metalloproteinases (MMPs) that are involved in tissue injury was found to be modulated by SRPP treatment in addition to increased cytoprotectivity due to enhanced synthesis of PGE(2) that necessitates the active proliferation of gastric mucin cells. Further, reduction in approximately 3 folds of galectin-3, an inflammatory marker suggests gastro protection against acid induced inflammation and gastric wall damages. Overall, studies show the effectiveness of SRPP in inhibiting MMPs and galectin-3 levels which were up-regulated during ulcer conditions. In addition SRPP ensured cytoprotectivity and rejuvenation of mucosal barrier via PGE(2) trigger leading to ulcer healing.