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撤除致动脉粥样化饮食对兔动脉粥样硬化斑块的影响。

Effects of withdrawing an atherogenic diet on the atherosclerotic plaque in rabbits.

作者信息

Zhao Lijun, Zhang Shifang, Su Qiaoli, Li Shuangqing

机构信息

Department of General Practice, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, P.R. China.

Department of Pulmonary Disease, Institute of Respiratory Disease, Chengdu Second People's Hospital, Chengdu, Sichuan 610000, P.R. China.

出版信息

Exp Ther Med. 2021 Jul;22(1):751. doi: 10.3892/etm.2021.10183. Epub 2021 May 12.

DOI:10.3892/etm.2021.10183
PMID:34035848
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8135140/
Abstract

Lifestyle interventions and pharmacotherapy are the most common of non-invasive treatments for atherosclerosis, but the individual effect of diet on plaques remains unclear. The current study aimed to investigate the effect of withdrawing the atherogenic diet on plaque in the aortas of rabbits. Experimental atheroma was induced in 33 rabbits using a 1% high cholesterol diet for 30 days (H-30 d) or 90 days (H-90 d, baseline group). After 90 days of the atherogenic diet, the remaining animals were divided into four groups: A total of 10 rabbits continued to consume the atherogenic diet for 50 days (H-90 d & H-50 d; n=5) or 140 days (H-90 d & H-140 d; n=5). Another 13 rabbits were switched to a chow diet for 50 days (H-90 d & C-50 d; n=7) or 140 days (H-90 d & C-140 d; n=6). A total of 10 age-matched rabbits in the control groups were fed a chow diet for 90 and 230 days, respectively. The or cross-sectional plaque areas were determined using oil red O staining and elastic van Gieson staining. Immunohistochemistry analyses were used to assess the macrophages or smooth muscle cell contents. When fed an atherogenic diet for 90 days, the rabbits' abdominal aortas exhibited severe atherosclerotic lesions (the median plaque area was 63.6%). After withdrawing the atherogenic diet, the plaque area did not shrink with feeding the chow diet compared with the baseline, but increased to 71.8 or 80.5% after 50 or 140 days, respectively. After removing cholesterol from the diet, the lipids content in the plaques increased during the first 50 days, and then decreased compared with the baseline group. Furthermore, withdrawing the atherogenic diet increased the total collagen content and the percentage of the smooth muscle cells, alleviated macrophage infiltration, decreased the vulnerable index and promoted the cross-linking of collagen. Feeding the rabbits an atherogenic diet followed by removal of cholesterol from the diet did not lead to the regression of established lesions but instead delayed the progression of the lesions and promoted the stabilization of the plaque.

摘要

生活方式干预和药物治疗是动脉粥样硬化最常见的非侵入性治疗方法,但饮食对斑块的个体影响仍不清楚。本研究旨在探讨去除致动脉粥样硬化饮食对兔主动脉斑块的影响。33只兔采用1%高胆固醇饮食诱导实验性动脉粥样硬化30天(H-30 d组)或90天(H-90 d组,即基线组)。致动脉粥样硬化饮食90天后,将其余动物分为四组:总共10只兔继续食用致动脉粥样硬化饮食50天(H-90 d & H-50 d组;n = 5)或140天(H-90 d & H-140 d组;n = 5)。另外13只兔改为普通饮食50天(H-90 d & C-50 d组;n = 7)或140天(H-90 d & C-140 d组;n = 6)。对照组中总共10只年龄匹配的兔分别喂食普通饮食90天和230天。使用油红O染色和弹性范吉森染色确定斑块面积或横截面斑块面积。免疫组织化学分析用于评估巨噬细胞或平滑肌细胞含量。当喂食致动脉粥样硬化饮食90天时,兔腹主动脉出现严重动脉粥样硬化病变(斑块面积中位数为63.6%)。去除致动脉粥样硬化饮食后,与基线相比,喂食普通饮食时斑块面积未缩小,但在50天或140天后分别增加至71.8%或80.5%。从饮食中去除胆固醇后,斑块中的脂质含量在最初50天内增加,然后与基线组相比下降。此外,去除致动脉粥样硬化饮食增加了总胶原蛋白含量和平滑肌细胞百分比,减轻了巨噬细胞浸润,降低了易损指数并促进了胶原蛋白的交联。给兔喂食致动脉粥样硬化饮食后再从饮食中去除胆固醇不会导致已形成病变的消退,反而会延迟病变进展并促进斑块稳定。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/76bf1459902c/etm-22-01-10183-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/f2e4dfeb76c3/etm-22-01-10183-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/bd694ed2ef6c/etm-22-01-10183-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/7dbcf5d30ad4/etm-22-01-10183-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/bce6ffc8e0a3/etm-22-01-10183-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/76bf1459902c/etm-22-01-10183-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/f2e4dfeb76c3/etm-22-01-10183-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/bd694ed2ef6c/etm-22-01-10183-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/7dbcf5d30ad4/etm-22-01-10183-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/bce6ffc8e0a3/etm-22-01-10183-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/490f/8135140/76bf1459902c/etm-22-01-10183-g04.jpg

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