Plain language summary
Helicobacter pylori infection is strongly associated with stomach cancer. Broccoli sprouts are rich in glucoraphanin, the precursor of sulforaphane and have been shown to be bactericidal against Helicobacter pylori infections. This study aimed to evaluate efficacy of broccoli sprouts in reducing H. pylori infection in high-salt, H. pylori–infected mice and infected humans. 6-wk-old mice were infected with H-Pylori and consumed a high salt diet for 2 months. High-salt diets exaggerate H. pylori–induced gastritis in mice. Mice were randomised into 2 groups receiving either broccoli sprouts in water or plain drinking water. Mice had free food access. 50 H. pylori–positive human volunteers whose endoscopy showed gastritis were randomised to consume 70 g/d of broccoli sprouts or equivalent of alfalfa sprouts for 8 weeks. Self reported compliance (95%) was confirmed by urine sample. In mice consuming the broccoli sprout water, inflammation was reduced, as were the cytokines unregulated by H. pylori infection. In humans, inflammation in the gastric lumen was significantly reduced in the broccoli sprout group only. Both stool and breath markers of H pylori were significantly lower when compared to control. The authors conclude that intake of sulforaphane-rich broccoli sprouts for 2 months reduces H. pylori colonization in mice and improves infection in H pylori positive mice and humans.
Abstract
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-alpha and interleukin-1beta, 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 micromol 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.
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