Protective and therapeutic potential of melatonin against intestinal diseases: updated review of current data based on molecular mechanisms

ABSTRACT

Introduction

Intestinal diseases, a leading global cause of mortality and morbidity, carry a substantial socioeconomic burden. Small and large intestines play pivotal roles in gastrointestinal physiology and food digestion. Pathological conditions, such as gut dysbiosis, inflammation, cancer, therapy-related complications, ulcers, and ischemia, necessitate the urgent exploration of safe and effective complementary therapeutic strategies for optimal intestinal health.

Areas covered

This article evaluates the potential therapeutic effects of melatonin, a molecule with a wide range of physiological actions, on intestinal diseases including inflammatory bowel disease, irritable bowel syndrome, colon cancer, gastric/duodenal ulcers and other intestinal disorders.

Expert opinion

Due to anti-inflammatory and antioxidant properties as well as various biological actions, melatonin could be a therapeutic option for improving digestive disorders. However, more researches are needed to fully understand the potential benefits and risks of using melatonin for digestive disorders.

KEYWORDS:

• Melatonin
• inflammatory bowel disease
• colon cancer
• irritable bowel syndrome
• ulcers
• gastrointestinal tract

Article highlights

• Melatonin is synthesized in the bowel and has therapeutic effects on intestinal diseases.

• Melatonin regulates the function and regeneration of epithelial cells.

• Melatonin modulates of immune cell response in the bowel.

• Melatonin decreases the tonicity of GI smooth muscles and secretion of gastric acid.

• Melatonin lessens gut microbiota dysbiosis.

Declaration of interests

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.