🧫 Role of Sulforaphane in Protecting the Gastrointestinal Tract Against H. pylori and NSAID-Induced Oxidative Stress

🌱 It is a reasonable assumption that sulforaphane protects the gastrointestinal mucosa from oxidative damage caused by Helicobacter pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs).

Last updated on 2025.10.08 (Posted on 2025.05.24)

📄 Paper Information

Title: Role of Sulforaphane in Protection of Gastrointestinal Tract Against H. pylori and NSAID-Induced Oxidative Stress
Authors: Akinori Yanaka et al.
Journal: Current Pharmaceutical Design, 2017
Link: PubMed


🔬 Background

Both Helicobacter pylori (H. pylori) infection and NSAID administration can induce oxidative stress in gastric and intestinal epithelial cells, leading to mucosal injury, gastritis, and intestinal damage.
Sulforaphane, abundant in cruciferous vegetables such as broccoli sprouts, is known for its antioxidant enzyme induction and anti-inflammatory properties.


🎯 Objective

To investigate whether sulforaphane can protect gastric and intestinal epithelial tissues against damage caused by H. pylori infection or NSAID exposure, using both animal models and human studies.


🧪 Methods

  • In vitro: Examined whether sulforaphane suppresses H. pylori viability and urease activity.
  • Animal experiments:
    • Induced gastritis in mice infected with H. pylori.
    • Induced small intestinal injury with NSAIDs.
    • Compared tissue damage between sulforaphane-treated and control groups.
  • Human trial:
    • Subjects infected with H. pylori consumed broccoli sprouts or a placebo.
    • Measured changes in infection density and gastric inflammation levels.

🧠 Results

In vitro: Sulforaphane inhibited H. pylori growth and urease enzyme activity.
Animal studies: The sulforaphane-treated group showed reduced gastritis severity and less NSAID-induced small intestinal injury.
Human trial: Broccoli sprout intake decreased H. pylori infection density and reduced gastric mucosal inflammation.


⚙️ Proposed Mechanisms

  • Antioxidant activation: Induction of phase II detoxifying enzymes reduces ROS accumulation.
  • Enhanced mucosal defense: Strengthens gastric protective mechanisms and decreases inflammatory cytokines.
  • Antibacterial effect: Partial inhibition of H. pylori growth and activity.

📌 Significance & Limitations

Significance:
This study provides evidence that sulforaphane offers protective effects beyond basic antioxidant action—potentially preventing or mitigating gastritis, intestinal epithelial injury, and H. pylori infection.
It supports sulforaphane’s potential as a nutritional adjunct for maintaining gastric health, especially in H. pylori–related or NSAID-induced damage.

Limitations:

  • Small-scale human trials → limited generalization.
  • Insufficient long-term safety data on dosage and consumption methods.
  • Lack of consideration for other gastrointestinal variables (e.g., diet, acid secretion, mucosal status).

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