Abstract | BACKGROUND: METHODS AND RESULTS: The anti- atherosclerosis effect of CRA in apolipoprotein E-deficient mice fed a Western-type diet was evaluated using atherosclerosis lesion area, serum profiles, gene expression and histological lesions. In vitro, the mechanisms responsible for the anti-inflammatory effect of CRA were investigated on a lipopolysaccharide-induced inflammation model. This model was also used to investigate in detail the effects of CRA on gene expression and nuclear factor (NF)-κB activation. Compared with the control group, the CRA-treated group exhibited a significant decrease in atherosclerotic lesion area, as well as expression of monocyte chemoattractant protein-1 (MCP-1) and CCR2. In vitro studies showed that CRA treatment downregulated the mRNA levels of MCP-1, and inhibited monocyte adhesion and migration, together with suppression of NF-κB signaling pathway. CONCLUSIONS: CRA is capable of ameliorating atherosclerosis in apolipoprotein E-deficient mice by, partly at least, inhibition of NF-κB activity along with decreased MCP-1 expression.
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Authors | Hong Chen, Jie Yang, Qin Zhang, Li-Hong Chen, Qiang Wang |
Journal | Circulation journal : official journal of the Japanese Circulation Society
(Circ J)
Vol. 76
Issue 4
Pg. 995-1003
( 2012)
ISSN: 1347-4820 [Electronic] Japan |
PMID | 22293444
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anti-Inflammatory Agents
- Apolipoproteins E
- Biomarkers
- CCL2 protein, human
- CCR2 protein, human
- Ccl2 protein, mouse
- Ccr2 protein, mouse
- Chemokine CCL2
- Inflammation Mediators
- Lipids
- Lipopolysaccharides
- NF-kappa B
- RNA, Messenger
- Receptors, CCR2
- Triterpenes
- corosolic acid
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Topics |
- Animals
- Anti-Inflammatory Agents
(pharmacology)
- Aorta
(drug effects, immunology, metabolism, pathology)
- Aortic Diseases
(blood, genetics, immunology, pathology, prevention & control)
- Apolipoproteins E
(deficiency, genetics)
- Atherosclerosis
(blood, genetics, immunology, pathology, prevention & control)
- Biomarkers
(blood)
- Cell Adhesion
(drug effects)
- Cell Line
- Cell Movement
(drug effects)
- Chemokine CCL2
(genetics, metabolism)
- Disease Models, Animal
- Dose-Response Relationship, Drug
- Humans
- Inflammation Mediators
(metabolism)
- Lipids
(blood)
- Lipopolysaccharides
(pharmacology)
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Monocytes
(drug effects, immunology, metabolism)
- NF-kappa B
(metabolism)
- RNA, Messenger
(metabolism)
- Receptors, CCR2
(genetics, metabolism)
- Signal Transduction
(drug effects)
- Time Factors
- Triterpenes
(pharmacology)
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