title: Astaxanthin-rich extract from the green alga Haematococcus pluvialis lowers plasma lipid concentrations and enhances antioxidant defense in apolipoprotein E knockout mice.
abstract: 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.
authors: Department of Nutritional Sciences, University of Connecticut, Storrs, CT, USA.
authors: Yue
authors: Y
authors: Yang
authors: Jeong Min
authors: JM
authors: Seo
authors: Anthony
authors: A
authors: Nguyen
authors: Tho X
authors: TX
authors: Pham
authors: Hea Jin
authors: HJ
authors: Park
authors: Youngki
authors: Y
authors: Park
authors: Bohkyung
authors: B
authors: Kim
authors: Richard S
authors: RS
authors: Bruno
authors: Jiyoung
authors: J
authors: Lee
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001057:Apolipoproteins E / Q000235:genetics* / Q000378:metabolism*; D000460:Chlorophyta / Q000737:chemistry*; D005786:Gene Expression Regulation / Q000187:drug effects; D008055:Lipids / Q000097:blood*; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D011973:Receptors, LDL / Q000235:genetics / Q000378:metabolism; D024341:Xanthophylls / Q000737:chemistry / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D001057:Apolipoproteins E; D008055:Lipids; D011973:Receptors, LDL; D024341:Xanthophylls; C005948:astaxanthine