title: Chitosan Oligosaccharides Attenuate Atherosclerosis and Decrease Non-HDL in ApoE-/- Mice.
abstract: OBJECTIVE
  Chitosan-oligosaccharides (COS) treatment showed lipid lowering effects in rats and reverse cholesterol transport (RCT) promotion in mice, suggested that COS might be a potential atheroprotective material. In this study, we investigated the effects of COS treatment on atherosclerosis (AS) in apolipoprotein E deficient mice (apoE-/-).
  
  
  METHODS
  After feeding high fat (HF) diet for 12 weeks with the gastric gavages administration of COS or vehicle, respectively, the mice were sacrificed for the assessment of atherosclerosis, plaque stability, and the mechanism investigation.
  
  
  RESULTS
  Cholesterol and TG in non-high density lipoprotein (non-HDL) fractions were reduced dramatically in COS groups. The COS treatment decreased the lesion areas of aortic enface, plaque areas in aortic root, and increased plaque stability in apoE-/-. Furthermore, the COS treatment significantly enhanced the expression of liver low density lipoprotein receptor (LDL-R), scavenger receptor BI (SR-BI) as well as the expression of macrophage SR-BI and ATP binding cassette transporter A1(ABCA1). We also found that the COS treatment did not affect the plasma lipid level in LDL-R deficient mice and cholesterol absorption in wild type mice.
  
  
  CONCLUSIONS
  COS treatment attenuated AS and decreased plasma non-HDL level in apoE-/-, and the potential mechanism might be involved with enhanced expression of hepatic LDL-R and SR-BI, and macrophage ABCA1.
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong; Institute of Atherosclerosis, Taishan Medical University.
authors.forename: Yang
authors.initials: Y
authors.lastname: Yu
authors.forename: Tian
authors.initials: T
authors.lastname: Luo
authors.forename: Shuai
authors.initials: S
authors.lastname: Liu
authors.forename: Guohua
authors.initials: G
authors.lastname: Song
authors.forename: Jiju
authors.initials: J
authors.lastname: Han
authors.forename: Yun
authors.initials: Y
authors.lastname: Wang
authors.forename: Shutong
authors.initials: S
authors.lastname: Yao
authors.forename: Lei
authors.initials: L
authors.lastname: Feng
authors.forename: Shucun
authors.initials: S
authors.lastname: Qin
mesh_terms: D064286:ATP Binding Cassette Transporter 1 / Q000378:metabolism; D000071018:ATP Binding Cassette Transporter, Subfamily G, Member 5; D018528:ATP-Binding Cassette Transporters / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics; D050197:Atherosclerosis / Q000378:metabolism* / Q000628:therapy*; D001692:Biological Transport; D002460:Cell Line; D048271:Chitosan / Q000737:chemistry / Q000627:therapeutic use*; D002784:Cholesterol / Q000097:blood / Q000235:genetics*; D008076:Cholesterol, HDL / Q000097:blood / Q000235:genetics*; D004195:Disease Models, Animal; D056945:Hep G2 Cells; D006801:Humans; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009844:Oligosaccharides / Q000737:chemistry / Q000627:therapeutic use*; D011973:Receptors, LDL / Q000378:metabolism; D051122:Scavenger Receptors, Class B / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
chemical_list: D064286:ATP Binding Cassette Transporter 1; D000071018:ATP Binding Cassette Transporter, Subfamily G, Member 5; D018528:ATP-Binding Cassette Transporters; D001057:Apolipoproteins E; D048271:Chitosan; D002784:Cholesterol; D008076:Cholesterol, HDL; D008055:Lipids; D008074:Lipoproteins; D020780:Matrix Metalloproteinase 9; D009844:Oligosaccharides; D011973:Receptors, LDL; D051122:Scavenger Receptors, Class B; D014280:Triglycerides; C577833:Abca1 protein, mouse; C462600:ABCG5 protein, mouse; C454739:Scarb1 protein, mouse; C501830:Mmp9 protein, mouse