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Thalidomide inhibits early atherogenesis in apoE-deficient mice

Chew, M; Zhou, J; Daugherty, A; Eriksson, Tommy LU ; Ellermann-Eriksen, S; Hansen, PR and Falk, E (2003) In Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS) 111(Suppl.). p.113-116
Abstract
Inflammation is present in all stages of atherosclerosis, from fatty streaks to rupture of mature plaques. Tumour necrosis factor (TNF)-alpha is expressed in atherosclerotic lesions but its role in atherogenesis has not been defined. To clarify the role of this cytokine, we administered thalidomide, a compound known to inhibit TNF-alpha production, to homozygous apolipoprotein E-deficient (apoE(-/-)) mice in order to examine the effect of thalidomide on the development of early atherosclerotic lesions. Twelve apoE(-/-) mice were randomized to receive either sustained-release thalidomide or placebo pellets implanted subcutaneously, and the amount of atherosclerosis was quantified six weeks later. Thalidomide was well tolerated and did not... (More)
Inflammation is present in all stages of atherosclerosis, from fatty streaks to rupture of mature plaques. Tumour necrosis factor (TNF)-alpha is expressed in atherosclerotic lesions but its role in atherogenesis has not been defined. To clarify the role of this cytokine, we administered thalidomide, a compound known to inhibit TNF-alpha production, to homozygous apolipoprotein E-deficient (apoE(-/-)) mice in order to examine the effect of thalidomide on the development of early atherosclerotic lesions. Twelve apoE(-/-) mice were randomized to receive either sustained-release thalidomide or placebo pellets implanted subcutaneously, and the amount of atherosclerosis was quantified six weeks later. Thalidomide was well tolerated and did not result in any changes in body weight. Mice treated with thalidomide had significantly smaller mean (7986+/-5189 vs 19607+/-10353 mum(2), p=0.05) and maximum (15800 [12777-23675] vs 37169 [28000-41351] mum(2), p=0.03) lesion sizes than those treated with placebo. Thus, thalidomide is capable of inhibiting the early development of atherosclerosis, presumably by inhibition of TNF-alpha secretion. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
pathology, inflammation, atherosclerosis, thalidomide, TNF-alpha, cytokines
in
Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS)
volume
111
issue
Suppl.
pages
113 - 116
publisher
John Wiley & Sons
external identifiers
  • wos:000183711200022
  • scopus:0037663818
ISSN
1600-0463
language
English
LU publication?
yes
id
d2549955-578e-494c-bf8f-facea35fff0a (old id 308303)
date added to LUP
2007-08-28 09:18:33
date last changed
2017-01-01 05:18:40
@article{d2549955-578e-494c-bf8f-facea35fff0a,
  abstract     = {Inflammation is present in all stages of atherosclerosis, from fatty streaks to rupture of mature plaques. Tumour necrosis factor (TNF)-alpha is expressed in atherosclerotic lesions but its role in atherogenesis has not been defined. To clarify the role of this cytokine, we administered thalidomide, a compound known to inhibit TNF-alpha production, to homozygous apolipoprotein E-deficient (apoE(-/-)) mice in order to examine the effect of thalidomide on the development of early atherosclerotic lesions. Twelve apoE(-/-) mice were randomized to receive either sustained-release thalidomide or placebo pellets implanted subcutaneously, and the amount of atherosclerosis was quantified six weeks later. Thalidomide was well tolerated and did not result in any changes in body weight. Mice treated with thalidomide had significantly smaller mean (7986+/-5189 vs 19607+/-10353 mum(2), p=0.05) and maximum (15800 [12777-23675] vs 37169 [28000-41351] mum(2), p=0.03) lesion sizes than those treated with placebo. Thus, thalidomide is capable of inhibiting the early development of atherosclerosis, presumably by inhibition of TNF-alpha secretion.},
  author       = {Chew, M and Zhou, J and Daugherty, A and Eriksson, Tommy and Ellermann-Eriksen, S and Hansen, PR and Falk, E},
  issn         = {1600-0463},
  keyword      = {pathology,inflammation,atherosclerosis,thalidomide,TNF-alpha,cytokines},
  language     = {eng},
  number       = {Suppl.},
  pages        = {113--116},
  publisher    = {John Wiley & Sons},
  series       = {Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS)},
  title        = {Thalidomide inhibits early atherogenesis in apoE-deficient mice},
  volume       = {111},
  year         = {2003},
}