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Roquinimex inhibits dextran sodium sulfate-induced murine colitis

Liu, Qing LU ; Wang, Yusheng LU ; Wan, MX; Zhang, XW; Andersson, G; Hedlund, G and Thorlacius, Henrik LU (2003) In Inflammation Research1995-01-01+01:00 52(2). p.64-68
Abstract
Objective: Roquinimex is a modulator of the immune system and has been shown to attenuate induction of several inflammatory and autoimmune diseases. The objective of the present study was to determine the efficacy of roquinimex in a model of murine colitis. Materials and methods: For this purpose, Balb/c mice were exposed to 5% dextran sodium sulfate (DSS) in the drinking water for five to six days. Roquinimex (300 mg kg(-1) day(-1)) was administered by subcutaneous (s.c.) injection 3 days prior to and throughout the treatment period with DSS. In separate experiments, 300 mg kg(-1) day(-1) of roquinimex was given therapeutically after initiation of DSS challenge. Results: DSS provoked clinical signs of colitis, reduced crypt height (CH)... (More)
Objective: Roquinimex is a modulator of the immune system and has been shown to attenuate induction of several inflammatory and autoimmune diseases. The objective of the present study was to determine the efficacy of roquinimex in a model of murine colitis. Materials and methods: For this purpose, Balb/c mice were exposed to 5% dextran sodium sulfate (DSS) in the drinking water for five to six days. Roquinimex (300 mg kg(-1) day(-1)) was administered by subcutaneous (s.c.) injection 3 days prior to and throughout the treatment period with DSS. In separate experiments, 300 mg kg(-1) day(-1) of roquinimex was given therapeutically after initiation of DSS challenge. Results: DSS provoked clinical signs of colitis, reduced crypt height (CH) and increased mucosal damage score (MDS) as analyzed by histology. In addition, challenge with DSS increased the colonic content of myeloperoxidase (MPO). Prophylactic administration of DSS-treated mice with roquinimex significantly reduced clinical signs of colitis, MDS and the CH-reduction. Moreover, in roquinimex treated animals, the MPO activity was significantly reduced by more than 50% compared to DSS control mice. Notably, therapeutic administration of roquinimex in DSS-treated mice also significantly inhibited the MDS, CH-reduction and MPO activity. Conclusions: These findings suggest that roquinimex strongly inhibits murine colitis and may provide a novel pharmacological approach to treat inflammatory bowel disease. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
leukocyte, TNF-alpha, colitis, inflammatory bowel disease
in
Inflammation Research1995-01-01+01:00
volume
52
issue
2
pages
64 - 68
publisher
Birkhaüser
external identifiers
  • wos:000181667400003
  • pmid:12665123
  • scopus:0037295215
ISSN
1420-908X
DOI
10.1007/s000110300002
language
English
LU publication?
yes
id
80e837ae-f673-49c7-8302-350d5324b5c5 (old id 315830)
date added to LUP
2007-09-17 10:58:21
date last changed
2018-05-29 11:10:43
@article{80e837ae-f673-49c7-8302-350d5324b5c5,
  abstract     = {Objective: Roquinimex is a modulator of the immune system and has been shown to attenuate induction of several inflammatory and autoimmune diseases. The objective of the present study was to determine the efficacy of roquinimex in a model of murine colitis. Materials and methods: For this purpose, Balb/c mice were exposed to 5% dextran sodium sulfate (DSS) in the drinking water for five to six days. Roquinimex (300 mg kg(-1) day(-1)) was administered by subcutaneous (s.c.) injection 3 days prior to and throughout the treatment period with DSS. In separate experiments, 300 mg kg(-1) day(-1) of roquinimex was given therapeutically after initiation of DSS challenge. Results: DSS provoked clinical signs of colitis, reduced crypt height (CH) and increased mucosal damage score (MDS) as analyzed by histology. In addition, challenge with DSS increased the colonic content of myeloperoxidase (MPO). Prophylactic administration of DSS-treated mice with roquinimex significantly reduced clinical signs of colitis, MDS and the CH-reduction. Moreover, in roquinimex treated animals, the MPO activity was significantly reduced by more than 50% compared to DSS control mice. Notably, therapeutic administration of roquinimex in DSS-treated mice also significantly inhibited the MDS, CH-reduction and MPO activity. Conclusions: These findings suggest that roquinimex strongly inhibits murine colitis and may provide a novel pharmacological approach to treat inflammatory bowel disease.},
  author       = {Liu, Qing and Wang, Yusheng and Wan, MX and Zhang, XW and Andersson, G and Hedlund, G and Thorlacius, Henrik},
  issn         = {1420-908X},
  keyword      = {leukocyte,TNF-alpha,colitis,inflammatory bowel disease},
  language     = {eng},
  number       = {2},
  pages        = {64--68},
  publisher    = {Birkhaüser},
  series       = {Inflammation Research1995-01-01+01:00},
  title        = {Roquinimex inhibits dextran sodium sulfate-induced murine colitis},
  url          = {http://dx.doi.org/10.1007/s000110300002},
  volume       = {52},
  year         = {2003},
}