Pediococcus acidilactici AS185 attenuates early atherosclerosis development through inhibition of lipid regulation and inflammation in rats. (September 2019)

• Record Type: Journal Article
• Authors: Wang, Chao; Wang, Han; Zhao, Zijian; Xiao, Shan; Zhao, Yujuan; Duan, Cuicui; Gao, Lei; Li, Shengyu; Wang, Jihui
• Is Part Of: Journal of functional foods. Volume 60(2019)
• Publication Date: 2019-09
• Subjects: Atherosclerosis -- Pediococcus acidilactici -- Probiotic -- Lipid profile -- Inflammation; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2019.103424
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: Pediococcus acidilactici AS185 (AS185), a probiotic, may prevent atherosclerosis. AS185 prevented dyslipidemia and inflammation in a rat model of AS. AS185 attenuated aortic pathology and inflammatory cytokines in a rat AS model. AS185 attenuated AS by reducing inflammation and altering unhealthy lipid profiles. Abstract: Pathophysiologic mechanisms underlying atherosclerosis (AS) development are linked to dyslipidemia and inflammation. Pediococcus acidilactici AS185, a probiotic, was isolated from traditional farmers' soybean paste (Yanji, China). This study aimed to assess P. acidilactici AS185 anti-atherosclerotic effects and elucidate molecular mechanisms of action using an early AS model of SD rats fed a high-fat diet with intraperitoneal vitamin D3 (VD3 ) injections. For 8 weeks, model rats received P. acidilactici AS185 via gavage once/day. Post-treatment serum levels of inflammatory mediators, lipids, adhesion molecules, aortic histopathological characteristics and AS-related aortic protein expression levels were assessed. P. acidilactici AS185 administration markedly increased serum HDL-C and IL-10 levels, while reducing serum TG, LDL-C, TC, Ox-LDL, ICAM-1, VCAM-1, TNF-α, IFN-γ, IL-1β, and IL-6 levels. Notably, P. acidilactici AS185 inhibited p-p38 and ERK1/2 MAPK pathways and decreased Ox-LDL and CD36 expression to attenuate early AS by altering lipid profiles and MAPK-signaling-based inflammation.