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Corosolic acid ameliorates atherosclerosis in apolipoprotein E-deficient mice by regulating the nuclear factor-κB signaling pathway and inhibiting monocyte chemoattractant protein-1 expression.

AbstractBACKGROUND:
Corosolic acid (CRA) is a pentacyclic triterpene acid that has been shown to exhibit an anti-atherosclerotic effect when added to diets of low-density lipoprotein-deficient mice, but the mechanisms are unclear. The purpose of the present study was to investigate the molecular mechanisms by which CRA ameliorates atherosclerosis.
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.
AuthorsHong Chen, Jie Yang, Qin Zhang, Li-Hong Chen, Qiang Wang
JournalCirculation journal : official journal of the Japanese Circulation Society (Circ J) Vol. 76 Issue 4 Pg. 995-1003 ( 2012) ISSN: 1347-4820 [Electronic] Japan
PMID22293444 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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
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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