Genistein attenuated gastric inflammation and apoptosis in Helicobacter pylori -induced gastropathy in rats
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RESEARCH ARTICLE
Open Access
Genistein attenuated gastric inflammation and apoptosis in Helicobacter pylori-induced gastropathy in rats Prasong Siriviriyakul1, Duangporn Werawatganon1* , Nisarat Phetnoo1, Kanjana Somanawat1, Tanittha Chatsuwan2, Naruemon Klaikeaw3 and Maneerat Chayanupatkul1
Abstract Background: Helicobacter 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. Methods: Eighteen 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). Results: Rats 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. Conclusion: Genistein 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. Keywords: Genistein, H. pylori, Apoptosis, Gastric inflammation, Gastropathy Background Helicobacter pylori (H. pylori) is a spiral-shaped gramnegative bacterium and a major player in the development of gastroduodenal diseases. The prevalence of H. *Correspondence: [email protected] 1 Department of Physiology, Faculty of Medicine, Alternative and Complementary Medicine for Gastrointestinal and Liver Diseases Research Unit, Chulalongkorn University, Bangkok 10330, Thailand Full list of author information is available at the end of the article
pylori infection ranges from 15 to 90% depending on the regions and the ethnicities [1]. Several studies demonstrated the association between H. pylori infection and numerous gastrointestinal diseases, such as chronic gastritis, peptic ulcer disease, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, and ga
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