Limits...
The Effects of Broccoli Sprout Extract Containing Sulforaphane on Lipid Peroxidation and Helicobacter pylori Infection in the Gastric Mucosa.

Chang YW, Jang JY, Kim YH, Kim JW, Shim JJ - Gut Liver (2015)

Bottom Line: 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.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.However, BSES prevented lipid peroxidation in the gastric mucosa and may play a cytoprotective role in H. pylori-induced gastritis.

View Article: PubMed Central - PubMed

Affiliation: Departments of Internal Medicine, Kyung Hee University College of Medicine, Seoul, Korea.

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 (13)C-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.

No MeSH data available.


Related in: MedlinePlus

Comparison of glutathione (GSH) concentrations in the gastric mucosal tissue before and after treatment in each group. There were no significant changes before or after the treatment in any of the three groups. GSH concentrations were increased slightly after broccoli sprout extract containing sulforaphane treatment in the subjects (group A+C), irrespective of their Helicobacter pylori infection status (p=0.332).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4477992&req=5

f2-gnl-09-486: Comparison of glutathione (GSH) concentrations in the gastric mucosal tissue before and after treatment in each group. There were no significant changes before or after the treatment in any of the three groups. GSH concentrations were increased slightly after broccoli sprout extract containing sulforaphane treatment in the subjects (group A+C), irrespective of their Helicobacter pylori infection status (p=0.332).

Mentions: In all 61 H. pylori (+) subjects, basal GSH concentrations were lower than those of the 28 H. pylori (−) subjects. However, the differences were not significant (p=0.526) (Table 3). GSH concentrations were increased slightly after BSES treatment, irrespective of H. pylori infection status (p=0.332) (Table 4, Fig. 2).


The Effects of Broccoli Sprout Extract Containing Sulforaphane on Lipid Peroxidation and Helicobacter pylori Infection in the Gastric Mucosa.

Chang YW, Jang JY, Kim YH, Kim JW, Shim JJ - Gut Liver (2015)

Comparison of glutathione (GSH) concentrations in the gastric mucosal tissue before and after treatment in each group. There were no significant changes before or after the treatment in any of the three groups. GSH concentrations were increased slightly after broccoli sprout extract containing sulforaphane treatment in the subjects (group A+C), irrespective of their Helicobacter pylori infection status (p=0.332).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4477992&req=5

f2-gnl-09-486: Comparison of glutathione (GSH) concentrations in the gastric mucosal tissue before and after treatment in each group. There were no significant changes before or after the treatment in any of the three groups. GSH concentrations were increased slightly after broccoli sprout extract containing sulforaphane treatment in the subjects (group A+C), irrespective of their Helicobacter pylori infection status (p=0.332).
Mentions: In all 61 H. pylori (+) subjects, basal GSH concentrations were lower than those of the 28 H. pylori (−) subjects. However, the differences were not significant (p=0.526) (Table 3). GSH concentrations were increased slightly after BSES treatment, irrespective of H. pylori infection status (p=0.332) (Table 4, Fig. 2).

Bottom Line: 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.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.However, BSES prevented lipid peroxidation in the gastric mucosa and may play a cytoprotective role in H. pylori-induced gastritis.

View Article: PubMed Central - PubMed

Affiliation: Departments of Internal Medicine, Kyung Hee University College of Medicine, Seoul, Korea.

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 (13)C-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.

No MeSH data available.


Related in: MedlinePlus