4.4 Article

Chitosan Oligosaccharides Attenuate Atherosclerosis and Decrease Non-HDL in ApoE-/- Mice

Journal

JOURNAL OF ATHEROSCLEROSIS AND THROMBOSIS
Volume 22, Issue 9, Pages 926-941

Publisher

JAPAN ATHEROSCLEROSIS SOC
DOI: 10.5551/jat.22939

Keywords

Chitosan oligosaccharides; Atherosclerosis; Scavenger receptor BI; Low density lipoprotein receptor; ATP binding cassette transporter A1

Funding

  1. Natural Science Foundation of China [81200216]
  2. National Basic Research Program of China [2007CB936104]
  3. Taishan Scholars Projects of Shandong Province [ZD056, ZD057]
  4. Shandong Province [BS2012YY034]
  5. Initializing Fund of Doctors in Taishan Medical University [2033]

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Aim: 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.

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