title: Compound K Attenuates the Development of Atherosclerosis in ApoE(-/-) Mice via LXRα Activation.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. zl1007@tmmu.edu.cn.|Department of pharmacy, Xinqiao Hospital &amp; The Second Affiliated Hospital, Third Military Medical University, Shapingba, Chongqing 400037, China. zl1007@tmmu.edu.cn.
authors.forename: Li
authors.initials: L
authors.lastname: Zhou
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. zhengyu@tmmu.edu.cn.
authors.forename: Yu
authors.initials: Y
authors.lastname: Zheng
authors.affiliation: Department of Outpatient, Logistical Engineering University of PLA, Shapingba, Chongqing 401311, China. jaiyi1979@163.com.
authors.forename: Zhuoying
authors.initials: Z
authors.lastname: Li
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. linn0626@163.com.
authors.forename: Lingxia
authors.initials: L
authors.lastname: Bao
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. douyin@tmmu.edu.cn.
authors.forename: Yin
authors.initials: Y
authors.lastname: Dou
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. tangyuan@tmmu.edu.cn.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Tang
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. jxz@tmmu.edu.cn.
authors.forename: Jianxiang
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. jazi@tmmu.edu.cn.
authors.forename: Jianzhi
authors.initials: J
authors.lastname: Zhou
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. liuya@tmmu.edu.cn.
authors.forename: Ya
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. jy@tmmu.edu.cn.
authors.forename: Yi
authors.initials: Y
authors.lastname: Jia
authors.affiliation: Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Shapingba, Chongqing 400038, China. xhl@tmmu.edu.cn.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Li
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics*; D050197:Atherosclerosis / Q000188:drug therapy* / Q000473:pathology; D020170:Caspase 1 / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000188:drug therapy; D005487:Foam Cells / Q000378:metabolism / Q000473:pathology; D036145:Ginsenosides / Q000494:pharmacology / Q000627:therapeutic use*; D000071518:Liver X Receptors / Q000378:metabolism*; D017737:Macrophages, Peritoneal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
chemical_list: D001057:Apolipoproteins E; D020170:Caspase 1; D002784:Cholesterol; D016207:Cytokines; D036145:Ginsenosides; D000071518:Liver X Receptors; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D051996:Transcription Factor RelA; D014280:Triglycerides; C112772:ginsenoside compound K
keywords: LXRα; atherosclerosis; compound K; inflammasome; reverse cholesterol transport