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Int. J. Mol. Sci. 2016, 17(7), 1054; doi:10.3390/ijms17071054

Compound K Attenuates the Development of Atherosclerosis in ApoE−/− Mice via LXRα Activation

1
Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China
2
Department of pharmacy, Xinqiao Hospital & The Second Affiliated Hospital, Third Military Medical University, Shapingba, Chongqing 400037, China
3
Department of Outpatient, Logistical Engineering University of PLA, Shapingba, Chongqing 401311, China
These authors contributed equally to this work
*
Authors to whom correspondence should be addressed.
Academic Editors: Michael Henein and Maurizio Battino
Received: 14 April 2016 / Revised: 27 June 2016 / Accepted: 28 June 2016 / Published: 8 July 2016
(This article belongs to the Section Bioactives and Nutraceuticals)
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Abstract

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 LXRα may contribute to the athero-protective effects of compound K. Conclusion: These observations provide evidence for an athero-protective effect of compound K via LXRα activation, and support its further evaluation as a potential effective modulator for the prevention and treatment of atherosclerosis. View Full-Text
Keywords: atherosclerosis; compound K; reverse cholesterol transport; inflammasome; LXRα atherosclerosis; compound K; reverse cholesterol transport; inflammasome; LXRα
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MDPI and ACS Style

Zhou, L.; Zheng, Y.; Li, Z.; Bao, L.; Dou, Y.; Tang, Y.; Zhang, J.; Zhou, J.; Liu, Y.; Jia, Y.; Li, X. Compound K Attenuates the Development of Atherosclerosis in ApoE−/− Mice via LXRα Activation. Int. J. Mol. Sci. 2016, 17, 1054.

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