Gastric-mucus penetrating and responsive microgels for alleviating Helicobacter pylori-induced gastritis

Xing Li1, Jipeng Zhang2, Xiangyu Liu1

  • 1Research Center of Food Colloids and Delivery of Functionality, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.

Insights

A novel microgel system effectively delivers sulforaphane (SFN) to combat Helicobacter pylori (H. pylori) infection. This gastric-responsive delivery enhances SFN

Area of Science:

  • Gastroenterology
  • Drug Delivery Systems
  • Microbiology

Background:

  • Helicobacter pylori (H. pylori) infection is a major cause of gastritis and gastric cancer worldwide.
  • Sulforaphane (SFN), a natural compound, shows promise against H. pylori but suffers from poor stability.
  • Effective delivery systems are needed to overcome SFN limitations for H. pylori treatment.

Purpose of the Study:

  • To develop a gastric-responsive microgel for targeted delivery of SFN against H. pylori.
  • To evaluate the stability, release kinetics, and efficacy of SFN-loaded microgels.
  • To assess the therapeutic potential of the microgel system in a mouse model of H. pylori infection.

Main Methods:

  • Chitosan-coated microgels (CTS-MGs) were fabricated using α-lactalbumin nanotubes loaded with SFN.
  • In vitro studies assessed SFN loading, gastric adhesion, and responsive release.
  • In vivo efficacy was evaluated in H. pylori-infected mice, assessing gastritis and gastric microbiota.

Main Results:

  • SFN-loaded CTS-MGs demonstrated high loading efficiency (10.73%) and strong gastric mucosal adhesion.
  • The microgels provided sustained SFN release in the stomach and penetrated mucus layers.
  • Oral administration of CTS-MG/SFN significantly reduced H. pylori load, alleviated gastritis, and restored gastric microbiota balance in mice.

Conclusions:

  • Gastric-responsive chitosan-coated microgels offer a promising strategy for oral delivery of SFN against H. pylori.
  • This delivery system enhances SFN's efficacy by improving gastric retention and targeted release.
  • The developed microgels hold potential for treating H. pylori infections and associated gastric diseases.

Related Concept Videos

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
272
Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
414
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
298
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
45
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
303
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
305