Thalidomide inhibits early atherogenesis in apoE-deficient mice
(2003) In APMIS : acta pathologica, microbiologica, et immunologica Scandinavica 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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/308303
- author
- Chew, M ; Zhou, J ; Daugherty, A ; Eriksson, Tommy LU ; Ellermann-Eriksen, S ; Hansen, PR and Falk, E
- organization
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- pathology, inflammation, atherosclerosis, thalidomide, TNF-alpha, cytokines
- in
- APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
- volume
- 111
- issue
- Suppl.
- pages
- 113 - 116
- publisher
- John Wiley & Sons Inc.
- 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
- 2016-04-01 12:37:35
- date last changed
- 2022-02-04 00:45:14
@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}},
keywords = {{pathology; inflammation; atherosclerosis; thalidomide; TNF-alpha; cytokines}},
language = {{eng}},
number = {{Suppl.}},
pages = {{113--116}},
publisher = {{John Wiley & Sons Inc.}},
series = {{APMIS : acta pathologica, microbiologica, et immunologica Scandinavica}},
title = {{Thalidomide inhibits early atherogenesis in apoE-deficient mice}},
volume = {{111}},
year = {{2003}},
}