Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 649, Issue 1-3, Pages 285-292Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2010.09.027
Keywords
WIN55212 2; Atherosclerosis; Inflammation; Macrophage
Categories
Funding
- Natural Science Foundation of China [30570732, 30871043, 30971219]
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The role of inflammation in all stages of atherosclerosis has been actively investigated with an emphasis on the discovery of novel and innovative drugs for treatment and prevention The anti-inflammatory and immunomodulatory capacity of cannabinoids are well established and these agents have a broad therapeutic potential in various inflammatory diseases including cardiovascular diseases The aim of this study was to investigate the effect of WIN55212 2 a synthetic cannabinoid on atherosclerosis using the apolipoprotein E knockout (ApoE(-/-)) mouse on a cholate containing high-fat diet Our results showed that WIN55212 2 reduced the size of atherosclerotic lesions in the aorta root and did not affect serum lipid levels significantly Furthermore alleviation of atherosclerosis by WIN55212-2 was associated with a smaller content of macrophages in plaque lesion as well as decreasing pro-inflammatory gene expression and NF kappa B activation in aortic tissues Oxidized LDL (ox LDL) dramatically induced NF kappa B activation and enhanced pro inflammatory mRNA and protein expression in peritoneal macrophages isolated from ApoE(-/-) mice It is noteworthy that all of the above mentioned effects of ox LDL were attenuated by WIN55212-2 Moreover WIN55212-2 also attenuated the inflammatory response that LPS induced AM630 a cannabinoid receptor 2 (CB2) special antagonist completely abolished the protective effects of WIN55212 2 both in vivo and in vitro Our data provide strong evidence that WIN55212 2 can potentially inhibit atherosclerosis in ApoE(-/-) mice Importantly all the beneficial effects of WIN55212 2 in our model were closely associated with the suppression of pro inflammatory responses and were mediated by the CB2 receptor (C) 2010 Elsevier B V All rights reserved
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