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中国圆田螺多糖通过调节载脂蛋白 E 缺陷小鼠肠道微生物群防治高脂饮食诱导的动脉粥样硬化的保护作用。

Protective activities of polysaccharides from Cipangopaludina chinensis against high-fat-diet-induced atherosclerosis via regulating gut microbiota in ApoE-deficient mice.

机构信息

Jiangsu Key Laboratory of Regional Resource Exploitation and Medicinal Research, Huaiyin Institute of Technology, Huai'an 223003, Jiangsu, China.

出版信息

Food Funct. 2019 Oct 16;10(10):6644-6654. doi: 10.1039/c9fo01530b.

Abstract

Sulfated polysaccharides (CCPS) obtained from Cipangopaludina chinensis have a certain protective effect on cardiovascular diseases, but whether they can slow down the development of atherosclerosis (AS) and how they work are still unclear. In this study, we aimed to determine the preventive effects of CCPS on high-fat-diet (HFD)-induced AS in mice and the underlying mechanism focusing on gut microbiota profile modulation. First, male apolipoprotein E knockout mice were fed HFD or normal diet and simultaneously intervened by a blank solvent, CCPS or atorvastatin to last for 12 weeks. Then, the histopathological characteristics, biochemical parameters and gut microbiota compositions of the experimental groups were compared. The results demonstrated that the CCPS supplementation significantly improved HFD-induced AS of the mice, which was mainly manifested by regulating the plasma lipid balance, decreasing the atherosclerotic index and reducing the atherosclerotic plaque area in a dose-dependent manner. Mechanistic analysis revealed that CCPS regulated the bacterial composition including reducing the ratio of Firmicutes/Bacteroidetes, decreasing the abundance of harmful bacteria and increasing the abundance of beneficial bacteria. Furthermore, through environmental factor correlation analysis, we found that the preventive effects of CCPS on AS in mice induced by HFD were closely related to reshaping the composition of gut microbiota.

摘要

从中国圆田螺中提取的硫酸多糖(CCPS)对心血管疾病有一定的保护作用,但它们是否能减缓动脉粥样硬化(AS)的发展以及如何发挥作用尚不清楚。在这项研究中,我们旨在确定 CCPS 对高脂饮食(HFD)诱导的小鼠动脉粥样硬化的预防作用及其潜在机制,重点是调节肠道微生物群谱。首先,雄性载脂蛋白 E 基因敲除小鼠用 HFD 或正常饮食喂养,并同时用空白溶剂、CCPS 或阿托伐他汀干预 12 周。然后,比较实验组的组织病理学特征、生化参数和肠道微生物群组成。结果表明,CCPS 补充剂显著改善了 HFD 诱导的小鼠动脉粥样硬化,主要表现为调节血浆脂质平衡、降低动脉粥样硬化指数和降低动脉粥样硬化斑块面积呈剂量依赖性。机制分析表明,CCPS 调节了细菌组成,包括降低厚壁菌门/拟杆菌门的比例、减少有害细菌的丰度和增加有益细菌的丰度。此外,通过环境因素相关性分析,我们发现 CCPS 对 HFD 诱导的小鼠动脉粥样硬化的预防作用与重塑肠道微生物群的组成密切相关。

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