The Effects of Broccoli Sprout Extract Containing Sulforaphane on Lipid Peroxidation and Helicobacter pylori Infection in the Gastric Mucosa.
- Author:
Young Woon CHANG
1
;
Jae Young JANG
;
Yong Ho KIM
;
Jung Wook KIM
;
Jae Jun SHIM
Author Information
- Publication Type:Original Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
- Keywords: Helicobacter pylori; Sulforaphane; Malondialde-hyde; Glutathione
- MeSH: Adult; Ammonia/metabolism; Antioxidants/*pharmacology; Biomarkers/analysis; Brassica/*chemistry; Breath Tests; Double-Blind Method; Enzyme-Linked Immunosorbent Assay; Female; Gastric Juice/enzymology; Gastric Mucosa/*drug effects/metabolism; Glutathione/analysis; Helicobacter Infections/*drug therapy; *Helicobacter pylori; Humans; Isothiocyanates/*pharmacology; Lipid Peroxidation/*drug effects; Male; Malondialdehyde/analysis; Middle Aged; Plant Extracts/chemistry/*pharmacology; Urea
- From:Gut and Liver 2015;9(4):486-493
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: The aims of this study were to investigate whether a broccoli sprout extract containing sulforaphane (BSES) inhibited the Helicobacter pylori infection density and exerted an antioxidative effect on gastric mucosal damage. METHODS: The enrolled subjects were randomized in a double-blinded manner into three groups. Finally, 33 H. pylori (+) BSES treatment subjects (group A), 28 H. pylori (+) placebo subjects (group B), and 28 H. pylori (-) BSES treatment subjects (group C) were studied. H. pylori infection density was indirectly quantified by a 13C-urea breath test (UBT), and the ammonia concentration in gastric juice aspirates was measured through gastroscopic examination. Malondialdehyde (MDA), an oxidative damage biomarker, and reduced glutathione (GSH), an antioxidant biomarker, were measured in the gastric mucosa by an enzyme-linked immunosorbent assay. RESULTS: BSES treatment did not significantly affect the UBT values or ammonia concentration in group A (p=0.634 and p=0.505, respectively). BSES treatment did significantly reduce mucosal MDA concentrations in group A (p<0.05) and group C (p<0.001), whereas the gastric mucosal GSH concentrations did not differ before and after treatment in any of the groups. CONCLUSIONS: BSES did not inhibit the H. pylori infection density. However, BSES prevented lipid peroxidation in the gastric mucosa and may play a cytoprotective role in H. pylori-induced gastritis.
