Compound K Attenuates the Development of Atherosclerosis in ApoE-/- Mice via LXR[alpha] Activation

Background: Atherosclerosis is a fundamental pathological process responded to some serious cardiovascular events. Although the cholesterol-lowering drugs are widely prescribed for atherosclerosis therapy, it is still the leading cause of death in the developed world. Here we measured the effects of...

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Bibliographic Details
Published in:International journal of molecular sciences 2016-07, Vol.17 (7), p.1054
Main Authors: Zhou, Li, Zheng, Yu, Li, Zhuoying, Bao, Lingxia, Dou, Yin, Tang, Yuan, Zhang, Jianxiang, Zhou, Jianzhi, Liu, Ya, Jia, Yi, Li, Xiaohui
Format: Article
Language:English
Subjects:
Atherosclerosis
Cardiovascular disease
Cholesterol
Pathology
Rodents
Online Access:Get full text
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Summary:Background: Atherosclerosis is a fundamental pathological process responded to some serious cardiovascular events. Although the cholesterol-lowering drugs are widely prescribed for atherosclerosis therapy, it is still the leading cause of death in the developed world. Here we measured the effects of compound K in atherosclerosis formation and investigated the probably mechanisms of the anti-antherosclerosis roles of compound K. Methods: We treated the atherosclerotic model animals (apoE-/- mice on western diet) with compound K and measured the size of atherosclerotic lesions, inflammatory cytokine levels and serum lipid profile. Peritoneal macrophages were collected in vitro for the foam cell and inflammasome experiments. Results: Our results show that treatment with compound K dose-dependently attenuates the formation of atherosclerotic plaques by 55% through activation of reverse cholesterol transport pathway, reduction of systemic inflammatory cytokines and inhibition of local inflammasome activity. Compound K increases the cholesterol efflux of macrophage-derived foam cells, and reduces the inflammasome activity in cholesterol crystal stimulated macrophages. The activation of LXR[alpha] may contribute to the athero-protective effects of compound K. Conclusion: These observations provide evidence for an athero-protective effect of compound K via LXR[alpha] activation, and support its further evaluation as a potential effective modulator for the prevention and treatment of atherosclerosis.
ISSN:1661-6596
1422-0067
DOI:10.3390/ijms17071054