Melatonin attenuates clock gene Cryptochrome1, which may aggravates mouse anti-type II collagen antibody-induced arthritis
Very recently, the circadian rhythm was proved to play an important role in the pathogenesis of arthritis. The role of melatonin in the development and progress of rheumatoid arthritis has been implicated for decades. This study was aimed to investigate the effect of melatonin on the expression of c...
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Published in | Rheumatology international Vol. 32; no. 2; pp. 379 - 385 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer-Verlag
01.02.2012
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Very recently, the circadian rhythm was proved to play an important role in the pathogenesis of arthritis. The role of melatonin in the development and progress of rheumatoid arthritis has been implicated for decades. This study was aimed to investigate the effect of melatonin on the expression of circadian
clock
genes in mouse anti-type II collagen antibody-induced arthritis (CIA). Mice were divided into 3 groups: control, CIA, and CIA + melatonin treatment (MLT). Both mRNA and protein levels of circadian
clock
gene
Cryptochrome1
(
Cry1
) were markedly decreased in CIA + MEL group compared with those in control and CIA groups. MLT increased paw thickness. Histologic and X-ray assessment also revealed increased infiltration of inflammatory cells, synovial hyperplasia, and the destruction of articular cartilage and bone by MLT. The concentrations of anti-type II collagen antibody in CIA + MEL group mice were significantly higher than those in control and CIA groups (
P
< 0.05). Serum concentrations of TNF-α (
P
< 0.005) and IL-6 (
P
< 0.05) in CIA + MLT group were also increased. Taken together, these results implicate that
clock
gene
Cry1
may be involved in the aggravation of MLT-mediated arthritis in mice anti-type II collagen antibody-induced arthritis. |
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ISSN: | 0172-8172 1437-160X |
DOI: | 10.1007/s00296-010-1641-9 |