Genistein attenuated gastric inflammation and apoptosis in Helicobacter pylori-induced gastropathy in rats

BackgroundHelicobacter pylori (H. pylori) infection is a major cause of chronic gastritis, peptic ulcer diseases and cancer. Genistein (4,5,7-trihydroxyisoflavone), a tyrosine-specific-protein kinase inhibitor, has been shown to exert an anti-inflammatory property. The aim of this study was to examine the treatment effects of genistein and its mechanisms in rats with H. pylori infection. MethodsEighteen male Sprague-Dawley rats were divided into three groups (6 rats per group): (1) control group (Con); (2) H. pylori infected group (HP): the rats were inoculated with H. pylori (10(8-)10(10)CFU/mL; 1mL/rat.) for 3 consecutive days; and (3) HP+genistein group (HP+Gen): the rats were inoculated with H. pylori as above. Then, they were gavaged with genistein (16mg/kg BW) for 14days. Gastric tissue was used for the determination of nuclear factor (NF)-kappa B expression by immunohistochemistry (IHC), degree of apoptosis by the terminal deoxynucleotidyl transferasemediated dUTP nick-end labeling (TUNEL) reaction, and histopathology. Serum samples were used to measure the levels of tumor necrosis factor-alpha (TNF-alpha) and cytokine-induced neutrophil chemoattractant-1 (CINC-1).ResultsRats in the HP group had significantly higher levels of pro-inflammatory mediators, NF-kappa B expression and apoptotic cells when compared with the Con group, and these markers significantly decreased in HP+Gen group when compared with the HP group. The histopathology of HP group showed moderate gastric inflammation and many HP colonization. Gastric pathology in HP+Gen group demonstrated the attenuation of inflammatory cell infiltration and H. pylori colonization.Conclusion Genistein exerted its gastroprotective effects through the reduction of pro-inflammatory mediators, nuclear receptor NF-kappa B expression and gastric mucosal apoptosis in rats with H. pylori-induced gastropathy.