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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 and liver · 34 citas

Cómo se estudió

Diseño
Ensayo controlado aleatorizado (indexado por PubMed)
Estudiado en
Personas
Resultado principal
Marcadores de salud y funcionamiento
Consumo medido con
No se indica

Quién lo pagó

Financiación
Financiación independiente
Universidad u hospital
Kyung Hee University
Subvenciones
Kyung Hee University (KHU-20071510)

Según 1 financiador declarado.

Publicación

Publicado
2014-10-06 · Gut Liver · vol. 9 · número 4 · pág. 486
Editorial
Korean Association for the Study of the Liver
Citado
54 citas · más que el 87% de estudios similares · 2.1× el promedio de su campo
Referencias
34 trabajos
Acceso
Acceso abierto (publicación gratuita) · CC-BY-NC
Áreas de investigación
Helicobacter pylori-related gastroenterology studies · Genomics, phytochemicals, and oxidative stress · Antioxidant Activity and Oxidative Stress
Palabras clave
broccoli sprout extract, sulforaphane, Helicobacter pylori infection, lipid peroxidation, gastric mucosa, malondialdehyde, reduced glutathione, oxidative stress, cytoprotection, 13C-urea breath test
MeSH
gastric mucosa, gastric juice, humans, helicobacter pylori, brassica, helicobacter infections, ammonia, malondialdehyde, isothiocyanates, sulfoxides, urea, glutathione, plant extracts, antioxidants, breath tests, enzyme-linked immunosorbent assay, double-blind method, lipid peroxidation, adult, middle aged, female, male, biomarkers

5 autores

  • Young Woon Chang🇰🇷Kyung Hee University
  • Jae Young Jang🇰🇷 · autor de correspondenciaKyung Hee University
  • Yong Ho Kim🇰🇷Kyung Hee University
  • Jung‐Wook Kim🇰🇷Kyung Hee University
  • Jae‐Jun Shim🇰🇷Kyung Hee University

Resumen

El texto original del estudio, en el idioma en que se publicó.

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.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY-NC).

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