This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Yanaka, A. Articles by Yamamoto, M. Search for Related Content PubMed PubMed Citation Articles by Yanaka, A. Articles by Yamamoto, M. Related Collections Clinical Intervention Clinical Intervention: Diet and Diet-related Factors Preclinical Intervention: In Vivo (Animals): Drugs, Nutritional Interventions, Mechanisms

Dietary Sulforaphane-Rich Broccoli Sprouts Reduce Colonization and Attenuate Gastritis in Helicobacter pylori–Infected Mice and Humans

Authors' Affiliations: ¹ Division of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Tokyo, Japan; ² Department of Gastroenterology, Graduate School of Comprehensive Human Sciences and ³ Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Japan; and ⁴ Department of Pharmacology and Molecular Sciences, School of Medicine, and Center for Human Nutrition, School of Public Health, Johns Hopkins University, Baltimore, Maryland

Requests for reprints: Akinori Yanaka, Division of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda-shi, Chiba-ken, 278-8510, Tokyo, Japan. Phone/Fax: 81-4-7121-3675; E-mail: ayanaka{at}rs.noda.tus.ac.jp.

The isothiocyanate sulforaphane [SF; 1-isothiocyanato-4(R)-methylsulfinylbutane] is abundant in broccoli sprouts in the form of its glucosinolate precursor (glucoraphanin). SF is powerfully bactericidal against Helicobacter pylori infections, which are strongly associated with the worldwide pandemic of gastric cancer. Oral treatment with SF-rich broccoli sprouts of C57BL/6 female mice infected with H. pylori Sydney strain 1 and maintained on a high-salt (7.5% NaCl) diet reduced gastric bacterial colonization, attenuated mucosal expression of tumor necrosis factor- and interleukin-1β, mitigated corpus inflammation, and prevented expression of high salt-induced gastric corpus atrophy. This therapeutic effect was not observed in mice in which the nrf2 gene was deleted, strongly implicating the important role of Nrf2-dependent antioxidant and anti-inflammatory proteins in SF-dependent protection. Forty-eight H. pylori–infected patients were randomly assigned to feeding of broccoli sprouts (70 g/d; containing 420 µmol of SF precursor) for 8 weeks or to consumption of an equal weight of alfalfa sprouts (not containing SF) as placebo. Intervention with broccoli sprouts, but not with placebo, decreased the levels of urease measured by the urea breath test and H. pylori stool antigen (both biomarkers of H. pylori colonization) and serum pepsinogens I and II (biomarkers of gastric inflammation). Values recovered to their original levels 2 months after treatment was discontinued. Daily intake of sulforaphane-rich broccoli sprouts for 2 months reduces H. pylori colonization in mice and improves the sequelae of infection in infected mice and in humans. This treatment seems to enhance chemoprotection of the gastric mucosa against H. pylori–induced oxidative stress.

Key Words: broccoli • glucoraphanin • Helicobacter