Daily Intake of Sulforaphane-Rich Broccoli Sprouts Suppresses H. pylori Colonization and Attenuates H. pylori-induced Gastritis via Upregulation of Nrf2-dependent Antixodaint Enzymes
10.1625/jcam.4.9
- VernacularTitle:スルフォラファン含有食品，ブロッコリースプラウト摂取によるＨ．ｐｙｌｏｒｉ胃炎軽減作用と胃癌予防の可能性
- Author:
Akinori YANAKA
;
Masafumi TAUCHI
;
Masayuki YAMAMOTO
;
Ichinosuke HYODO
- Publication Type:Journal Article
- Keywords:
broccoli sprout;
sulforaphane;
Helicobacter pylori;
gastritis;
oxidative stress
- From:Japanese Journal of Complementary and Alternative Medicine
2007;4(1):9-15
- CountryJapan
- Language:Japanese
-
Abstract:
Background: Sulforaphane (SFN), a compound abundant in broccoli sprouts (BS), protects cells from oxidative injury by activating nrf2-mediated antioxidant enzymes. Sulforaphane also shows bactericidal activity against H. pylori in vitro. The aim of this study was to determine if daily intake of SFN-rich BS inhibits H. pylori colonization and mitigated gastritis in H. pylori-infected gastric mucosa in mice and humans.
Methods: Study 1: Nrf2+/+ and nrf2−/− C57BL/6 female mice were infected with H.pylori Sydney Strain; SS1. Mice were maintained for 2 mo. on a high salt diet (7.5% NaCl), supplemented with or without BS containing approximately 2.5 mM SFN. Degree of gastritis was evaluated by updated Sydney system. Study 2: Fifty subjects infected with H. pylori were randomly assigned to either the BS group (n=25) or the Alfalfa Sprouts (AS) group (n=25). All subjects were asked to eat BS 70 g/day (containing approximately 180 mg SFN) or AS 70 g/day (no SFN) for 2 months. H.pylori colonization was evaluated by measurement of HpSA. The degree of gastritis was evaluated by measuring serum levels of pepsinogen (PG) I and II.
Results: Study 1: BS treatment decreased Hp colonization and mitigated gastritis in nrf2+/+ but not in nrf2−/− mice. Study 2: Two months intervention with BS decreased HpSA values and serum levels of PG I and II, while AS showed on effect.
Conclusion: Daily intake of SFN-rich BS suppresses H.pylori colonization and improves gastritis in H. pylori-infected gastric mucosa via nrf2-dependent mechanisms.
