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失调的微生物群落导致大鼠急性心肌梗死的严重程度增加。

Dysbiotic microbiota contributes to the extent of acute myocardial infarction in rats.

机构信息

Research Center, CIUSSS du Nord-de-l'Île-de-Montréal, Hôpital Sacré-Cœur, Montreal, Canada.

Department of Pharmacology and Physiology, Université de Montréal, Montreal, Canada.

出版信息

Sci Rep. 2022 Oct 3;12(1):16517. doi: 10.1038/s41598-022-20826-z.

DOI:10.1038/s41598-022-20826-z
PMID:36192578
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9530207/
Abstract

Increasing evidence suggests that the intestinal microbiota composition could play a role in specific pathologies such as hypertension, obesity and diabetes. This study aims to demonstrate that the intestinal microbiota modulated by a diet creating dysbiosis increased the size of the myocardial infarction and that probiotics could attenuate this effect. To do this, microbiota transplants from rats fed a dysbiotic or non-dysbiotic diet in the presence or absence of probiotics were performed for 10 days on rats whose microbiota had been previously suppressed by antibiotic therapy. Then, the anterior coronary artery of the transplanted rats was occluded for 30 min. Infarct size was measured after 24 h of reperfusion, while signaling pathways were evaluated after 15 min of reperfusion. Intestinal resistance, plasma concentration of LPS (lipopolysaccharides), activation of NF-κB and Akt and composition of the microbiota were also measured. Our results demonstrate a larger infarct size in animals transplanted with the dysbiotic microbiota without probiotics compared to the other groups, including those that received the dysbiotic microbiota with probiotics. This increase in infarct size correlates with a higher firmicutes/bacteroidetes ratio, NF-kB phosphorylation and plasma LPS concentration, and a decrease in intestinal barrier resistance and Akt. These results indicate that dysbiotic microbiota promotes an increase in infarct size, an effect that probiotics can attenuate.

摘要

越来越多的证据表明,肠道微生物群落的组成可能在某些特定疾病中发挥作用,如高血压、肥胖和糖尿病。本研究旨在证明通过饮食引起的肠道微生物群落失调会增加心肌梗死的面积,而益生菌可以减轻这种影响。为此,将喂食失调或非失调饮食的大鼠的微生物群落移植到先前通过抗生素治疗抑制其微生物群落的大鼠身上,持续 10 天。然后,将移植大鼠的前冠状动脉闭塞 30 分钟。在再灌注 24 小时后测量梗死面积,而在再灌注 15 分钟后评估信号通路。还测量了肠道阻力、血浆 LPS(脂多糖)浓度、NF-κB 和 Akt 的激活以及微生物群落的组成。我们的结果表明,与其他组相比,未用益生菌移植失调微生物群落的动物的梗死面积更大,包括那些接受失调微生物群落加益生菌的动物。这种梗死面积的增加与较高的厚壁菌门/拟杆菌门比值、NF-κB 磷酸化和血浆 LPS 浓度以及肠道屏障阻力和 Akt 的降低相关。这些结果表明,失调的微生物群落促进了梗死面积的增加,而益生菌可以减轻这种影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/b92be72a2aa5/41598_2022_20826_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/dbbd76153dba/41598_2022_20826_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/33ab1e182ed2/41598_2022_20826_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/542ac4c5090b/41598_2022_20826_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/b92be72a2aa5/41598_2022_20826_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/dbbd76153dba/41598_2022_20826_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/33ab1e182ed2/41598_2022_20826_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/542ac4c5090b/41598_2022_20826_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f76a/9530207/b92be72a2aa5/41598_2022_20826_Fig4_HTML.jpg

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