Abstract
There is an increasing interest in the effect of dietary polyphenols on the intestinal microbiota and the possible associations between this effect and the development of some cardiovascular diseases, such as atherosclerosis (AS). However, limited information is available on how these polyphenols affect the gut microbiota and AS development. This study was designed to evaluate the modulation of dietary tea polyphenols (TPs) on intestinal Bifidobacteria (IB) and its correlation with AS development in apolipoprotein E-deficient (ApoE−/−) mice. Fifty C57BL/6 ApoE−/− mice were randomized into one of the five treatment groups (n = 10/group): control group fed normal diet (CK); a group fed a high-fat diet (HFD); and the other three groups fed the same HFD supplemented with TPs in drinking water for 16 weeks. The total cholesterol and low-density lipoprotein cholesterol (LDL-C) were decreased significantly (P < 0.05) after TP interference. In addition, the TP diet also decreased the plaque area/lumen area (PA/LA) ratios (P < 0.01) in the TP diet group. Interestingly, copies of IB in the gut of ApoE−/− mice were notably increased with TP interference. This increase was dose dependent (P < 0.01) and negatively correlated with the PA/LA ratio (P < 0.05). We conclude that TPs could promote the proliferation of the IB, which is partially responsible for the reduction of AS plaque induced by HFD.
Highlights
Atherosclerosis (AS) is a leading cause of death in Western countries, which is a complex pathophenotype governed by genetic and environmental determinants
The results indicated an association between the fat content in the feed and development of AS lesions: the plaque area/lumen area (PA/LA) ratio in the high-fat diet (HFD) group was 0.69 ± 0.18, whereas no AS plaques were observed in the normal diet group (CK) group
low-density lipoprotein cholesterol (LDL-C) is the most significant risk factor for AS development: LDL-C can be oxidized into ox-LDL, which may interact with the scavenger receptors of macrophages and vascular smooth muscle membranes in the arterial wall
Summary
Atherosclerosis (AS) is a leading cause of death in Western countries, which is a complex pathophenotype governed by genetic and environmental determinants. High-fat diet (HFD) is one of the environmental risk factors for the development of AS, which may cause changes in the intestinal microbial communities and may lead to obesity and low-grade intestinal inflammation [1]. The gut microbiota itself is an environmental risk factor for the development of AS [2]. Intestinal microbial communities may influence the efficiency of dietary energy uptake and influence susceptibility to obesity. A novel pathway linking dietary lipid intake, intestinal microbiota, and AS was identified, and the regulation of surface expression levels of macrophage scavenger receptors is well known to participate in the atherosclerotic process [3]. Gut microbiota is believed to be responsible for the control of metabolic endotoxemia, low-grade inflammation, and obesity [4]. Infection of Helicobacter cinaedi was found to alter expression of cholesterol receptors and transporters in cultured macrophages and caused foam cell formation, and enhanced AS in hyperlipidemic mice [7]
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