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Abstract Title:

Compound K Attenuates the Development of Atherosclerosis in ApoE(-/-) Mice via LXRα Activation.

Abstract Source:

Int J Mol Sci. 2016 Jul 8 ;17(7). Epub 2016 Jul 8. PMID: 27399689

Abstract Author(s):

Li Zhou, Yu Zheng, Zhuoying Li, Lingxia Bao, Yin Dou, Yuan Tang, Jianxiang Zhang, Jianzhi Zhou, Ya Liu, Yi Jia, Xiaohui Li

Article Affiliation:

Li Zhou

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.

Study Type : Animal Study

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