AI Article Synopsis

  • Inflammatory bowel disease (IBD) is chronic inflammation of the gastrointestinal tract, worsened by stress like sleep deprivation, and can be treated with melatonin.
  • A study using a mouse model of colitis showed that sleep deprivation led to weight loss and increased disease severity, while melatonin helped reduce inflammation.
  • The research identified specific genes such as adiponectin and aquaporin 8 affected by sleep deprivation and melatonin treatment, suggesting their roles in inflammation regulation.

Article Abstract

Background: Inflammatory bowel disease is a chronic inflammatory condition of the gastrointestinal tract. It can be aggravated by stress, like sleep deprivation, and improved by anti-inflammatory agents, like melatonin. We aimed to investigate the effects of sleep deprivation and melatonin on inflammation. We also investigated genes regulated by sleep deprivation and melatonin.

Methods: In the 2% DSS induced colitis mice model, sleep deprivation was induced using modified multiple platform water bath. Melatonin was injected after induction of colitis and colitis with sleep deprivation. Also mRNA was isolated from the colon of mice and analyzed via microarray and real-time PCR.

Results: Sleep deprivation induced reduction of body weight, and it was difficult for half of the mice to survive. Sleep deprivation aggravated, and melatonin attenuated the severity of colitis. In microarrays and real-time PCR of mice colon tissues, mRNA of adiponectin and aquaporin 8 were downregulated by sleep deprivation and upregulated by melatonin. However, mRNA of E2F transcription factor (E2F2) and histocompatibility class II antigen A, beta 1 (H2-Ab1) were upregulated by sleep deprivation and downregulated by melatonin.

Conclusion: Melatonin improves and sleep deprivation aggravates inflammation of colitis in mice. Adiponectin, aquaporin 8, E2F2 and H2-Ab1 may be involved in the inflammatory change aggravated by sleep deprivation and attenuated by melatonin.

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Source
http://dx.doi.org/10.1007/s10620-013-3013-2DOI Listing

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