Abstract
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 (108− 1010 CFU/mL; 1 mL/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 (16 mg/kg BW) for 14 days. Gastric tissue was used for the determination of nuclear factor (NF)-κB 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-α) and cytokine-induced neutrophil chemoattractant-1 (CINC-1).ResultsRats in the HP group had significantly higher levels of pro-inflammatory mediators, NF-κB 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.ConclusionGenistein exerted its gastroprotective effects through the reduction of pro-inflammatory mediators, nuclear receptor NF-κB expression and gastric mucosal apoptosis in rats with H. pylori-induced gastropathy.
Highlights
Helicobacter pylori (H. pylori) infection is a major cause of chronic gastritis, peptic ulcer diseases and cancer
We aimed to evaluate the anti-inflammatory effects of genistein, which may attenuate gastropathy through the suppression of nuclear receptor nuclear factor (NF)-κB expression, pro-inflammatory mediator production (i.e. Tumor necrosis factor-alpha (TNF-α) and cytokine-induced neutrophil chemoattractant-1 (CINC-1)), and gastric epithelial cell apoptosis in rats with H. pylori infection
Changes in levels of pro‐inflammatory mediators, serum TNF‐α and CINC‐1 As shown in Fig. 1a and b, the H. pylori infected group (HP) group had significantly higher levels of serum TNF-α and CINC-1 when compared with the control group (Con) group (47.92 ± 13.74 pg/mL vs. 18.95 ± 7.94 pg/mL and 137.28 ± 47.67 pg/mL vs. 72.27 ± 6.07 pg/mL, respectively, P < 0.05)
Summary
Helicobacter pylori (H. pylori) infection is a major cause of chronic gastritis, peptic ulcer diseases and cancer. The bacteria inject its virulent factors, cagA protein, into the host epithelial cells using the type IV secretory system [3, 5]. These virulent factors affect host epithelial cell cytoskeletal rearrangements and activate NF-kB pathway, which subsequently induce IL-8 expression and release [6,7,8]. IL-8 is a potent chemotactic factor, attracting neutrophils and lymphocytes to the affected area These inflammatory cells release pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and IL-6 leading to gastric mucosal injury and gastric epithelial cell apoptosis [9,10,11]. In response to TNF-α stimulation, gastric epithelial cells release cytokine-induced neutrophil chemoattractant-1 (CINC-1) which works in concert with IL-8 in the attraction of neutrophils adding further insults to the injured mucosa [12]
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