Melatonin alters amino acid metabolism and inflammatory responses in colitis mice

Amino Acids. 2017 Dec;49(12):2065-2071. doi: 10.1007/s00726-017-2489-z. Epub 2017 Sep 19.

Abstract

Inflammatory bowel disease is a chronic inflammatory dysfunction of the gastrointestinal tract. This study explored the hypothesis that melatonin has beneficial functions in the mouse model of colitis induced by dextran sodium sulfate (DSS), with a specific focus on the expression of intestinal inflammatory cytokines and the serum levels of amino acids. The results revealed that mice with melatonin supplementation had a reduction in weight loss and disease index induced by DSS treatment. Melatonin stifled the expression of colonic IL-17 in mice with DSS-induced colitis. Melatonin also lowered the serum levels of Asp, Ser, Met, and Leu (p < 0.05), but increased those of Glu and Cys (p < 0.05). Thus, melatonin treatment is promising and may function as a potential adjuvant therapy to alleviate the clinical symptoms of patients with inflammatory bowel disease.

Keywords: Glutamine; IL-17; Inflammatory bowel disease; Melatonin; TNF-α.

MeSH terms

  • Amino Acids / blood
  • Amino Acids / metabolism*
  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Body Weight / drug effects
  • Colitis / blood
  • Colitis / chemically induced
  • Colitis / drug therapy
  • Colitis / physiopathology*
  • Dextran Sulfate
  • Disease Models, Animal
  • Gene Expression Regulation / drug effects*
  • Interleukin-17 / genetics
  • Melatonin / pharmacology*
  • Mice
  • Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Amino Acids
  • Anti-Inflammatory Agents
  • Interleukin-17
  • Tumor Necrosis Factor-alpha
  • Dextran Sulfate
  • Melatonin