Oral administration of the β-glucan produced by Aureobasidium pullulans ameliorates development of atherosclerosis in apolipoprotein E deficient mice. (October 2015)

• Record Type: Journal Article
• Authors: Aoki, Shiho; Iwai, Atsushi; Kawata, Koji; Muramatsu, Daisuke; Uchiyama, Hirofumi; Okabe, Mitsuyasu; Ikesue, Masahiro; Maeda, Naoyoshi; Uede, Toshimitsu
• Is Part Of: Journal of functional foods. Volume 18:Part A(2016)
• Page Start: 22
• Page End: 27
• Publication Date: 2015-10
• Subjects: ApoE apolipoprotein E -- AP-PG A. pullulans-produced β-glucan -- CAD coronary artery disease -- HDL high-density lipoprotein -- HFD high-fat diet -- LDL low-density lipoprotein -- ox-LDL oxidized low-density lipoprotein; β-glucan -- Aureobasidium pullulans -- Atherosclerosis; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2015.06.044
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: Aureobasidium pullulans -derived β-glucan (AP-PG) is known to be an immunomodulator. Apolipoprotein E deficient (ApoE) mice spontaneously develop atherosclerosis. AP-PG is effective in ameliorating development of atherosclerosis in the model mice. AP-PG administration reduces oxidized low-density lipoprotein cholesterol levels. Oral administration of AP-PG ameliorates vascular accumulation of macrophages. Abstract: The Aureobasidium pullulans -produced β-glucan (AP-PG) is an immune stimulator, and believed to exhibit beneficial effects on health through its immune stimulating activity. Here, the effect of oral administration of AP-PG on high-fat diet (HFD)-induced atherosclerosis was evaluated using apolipoprotein E deficient mice, a widely used mouse model for atherosclerosis. The results demonstrated that HFD-induced development of atherosclerosis was significantly reduced in the AP-PG-treated mice when compared with that of the control mice. In serological analysis, blood levels of oxidized low-density lipoprotein cholesterol, a well-known risk factor for the development of atherosclerosis, were significantly reduced in the AP-PG-treated group of mice. Further, immunohistochemical analysis using MOMA-2 antibody showed that oral administration of AP-PG is effective in ameliorating vascular accumulation of macrophages. These data suggest the possibility that oral administration of AP-PG is effective in ameliorating HFD-induced development of atherosclerosis.