Protective effects of Weilikang decoction on gastric ulcers and possible mechanisms

Although Weilikang decoction (WLK) has been used for gastric ulcer (GU) therapy in a clinical setting with good curative effect for >20 years, the mechanism remains unclear. Several GU animal models, induced by ethanol, hydrochloric acid, aspirin, pylorus ligation, acetic acid and indomethacin, were used to investigate the gastroprotective effects of WLK decoction. Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), indomethacin, and N-ethylmaleimide (NEM) were pretreated, respectively, to investigate the action mechanism. Real-time polymerase chain reaction and Western blot analysis methods were used to determine the effects of WLK on indomethacin-induced GUs. The WLK-administered groups (2.5, 1.25 and 0.625 g/kg) significantly reduced the GU areas induced by ethanol, hydrochloric acid and aspirin. Furthermore, the effects could be quenched by L-NAME and NEM, but not by indomethacin. The 2.5 and 1.25 g/kg WLK groups showed significantly decreased effects on GU areas induced by pylorus ligation and acetic acid. WLK treatment significantly decreased mRNA expression on cyclooxygenase (COX)-1, COX-2, interleukin-6, tumor necrosis factor α and inducible nitric oxide synthase (iNOS) mRNA, but showed no effect on endothelial nitric oxide synthase mRNA expression. Western blot analysis result showed that WLK-treated groups markedly downregulated COX-2 protein expression. The anti-ulcer potential of WLK can be primarily attributed to its regulatory effects on nitric oxide, sulfhydryl compounds, and reduction effect on mucosal expression of proinflammatory cytokines.