Astaxanthin-rich extract from the green alga Haematococcus pluvialis lowers plasma lipid concentrations and enhances antioxidant defense in apolipoprotein E knockout mice

J Nutr. 2011 Sep;141(9):1611-7. doi: 10.3945/jn.111.142109. Epub 2011 Jul 6.


Dyslipidemia and oxidative stress contribute to atherogenesis. Astaxanthin (ASTX) is a red-colored carotenoid well known for its high antioxidant capacity. However, its effects on lipid metabolism and antioxidant defense mechanisms have received only limited investigation. We fed male apoE knockout (apoE)(-/-) mice, a mouse model for atherosclerosis, a high-fat (15%)/high-cholesterol (0.2%) diet alone (control) or supplemented with ASTX-rich Hematococcus pluvialis extract (0.03% ASTX by weight) for 4 wk. ASTX-fed apoE(-/-) mice had significantly lower plasma total cholesterol and TG concentrations than controls, but body weight and plasma alanine aminotransferase and aspartate aminotransferase did not differ between the groups. qRT-PCR analysis demonstrated significantly greater mRNA levels of LDL receptor (LDLR), 3-hydroxy-3-methylglutaryl CoA reductase, and sterol regulatory element binding protein 2 (SREBP-2) and greater mature SREBP-2 protein in the livers of ASTX-fed mice, indicating that increased LDLR expression may be responsible for the hypocholesterolemic effect of ASTX. Hepatic lipogenic gene expression was not altered, but carnitine palmitoyl transferase 1, acetyl-CoA carboxylase β, and acyl-CoA oxidase mRNA abundance were significantly increased by ASTX supplementation, suggesting the TG-lowering effect of ASTX may be due to increased fatty acid β-oxidation in the liver. Expression of the nuclear factor E2 related factor 2-responsive endogenous antioxidant gene also was induced with concomitantly lower glutathione disulfide levels in the livers of ASTX-fed apoE(-/-) mice compared to controls. In conclusion, these results suggest that supplementation of ASTX-rich H. pluvialis extract improves cholesterol and lipid metabolism as well as antioxidant defense mechanisms, all of which could help mitigate the progression of atherosclerosis.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Apolipoproteins E / genetics*
  • Apolipoproteins E / metabolism*
  • Chlorophyta / chemistry*
  • Gene Expression Regulation / drug effects
  • Lipids / blood*
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Knockout
  • Receptors, LDL / genetics
  • Receptors, LDL / metabolism
  • Xanthophylls / chemistry
  • Xanthophylls / pharmacology


  • Antioxidants
  • Apolipoproteins E
  • Lipids
  • Receptors, LDL
  • Xanthophylls
  • astaxanthine