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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


EXPERIMENTAL CHRONIC COLITIS IN MICE IS MODIFIED BY MELATONIN TREATMENT
Abstract number: OTH16-62

Golab1 M., Dudziak1 M., Majewski1 P., Skwarlo-Sonta1 K.

1Department of Animal Physiology, Faculty of Biology, University of Warsaw, [email protected]

Aim: 

The aim of this study was to examine the immunomodulatory properties of melatonin administered to mice with experimental colitis.

Methods: 

Experiment was conducted on 6-8 week-old male BALB/c mice, maintained in standard laboratory conditions, LD 12:12. Chronic colitis was induced by 1% dextran sulfate sodium (DSS) solution, administered in drinking water for 3 weeks. Mice were treated daily with melatonin (10 mg/kg b.w.) by gavage, either from the beginning of experiment or after positive occult blood tests recording. Mice were killed by CO2 asphyxia in ZT 6 and ZT 18 (i.e. mid-day and mid-night, respectively). Peritoneal cavity was flushed with PBS, peritoneal leunited kingdomocytes (PTL) were counted and their reactive oxygen species (ROS) production was measured. Colons were dissected out and used for histological tests.

Results: 

In mice without colitis melatonin treatment caused cell proliferation in gut lymphatic nodules. DSS administration resulted in crypt shortening and loss with subsequent intensive mononuclear cells infiltration to the mucosa. Melatonin administration did not prevent inflammatory infiltration, but crypt loss location either in proximal or distal part of the colon depended on the length of melatonin treatment. PTL number was elevated in mice with colitis only during the light phase, and was not modified by melatonin treatment. ROS production by PTL was elevated by preventive melatonin only during the night.

Conclusion: 

These preliminary results show a possible protective action of the orally administered melatonin in the gut, dependent on the length of the treatment period.

Supported by Polish MSHE grant 2P04C 117 29.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :OTH16-62

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