Spermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-3

Spermidine, which can be synthesized by the gut microbiota, can prevent cardiac hypertrophy and delay the progression to heart failure (HF). However, it is not clear whether the effect of spermidine on cardiac function is mediated by modulating the gut microbiota when HF occurs. Female HF Kunming mi...

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Autores principales: Yufeng Chen, Zhiqin Guo, Shaonan Li, Zhen Liu, Pingan Chen
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Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/14d2dab2f2824d2592143a09aea413d7
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spelling oai:doaj.org-article:14d2dab2f2824d2592143a09aea413d72021-12-02T08:04:23ZSpermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-32297-055X10.3389/fcvm.2021.765591https://doaj.org/article/14d2dab2f2824d2592143a09aea413d72021-12-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcvm.2021.765591/fullhttps://doaj.org/toc/2297-055XSpermidine, which can be synthesized by the gut microbiota, can prevent cardiac hypertrophy and delay the progression to heart failure (HF). However, it is not clear whether the effect of spermidine on cardiac function is mediated by modulating the gut microbiota when HF occurs. Female HF Kunming mice induced by transverse aortic constriction were administered spermidine (HF+S group) or its antagonist (HF+SR group). Echocardiography, messenger ribonucleic acid (RNA) and protein expression of galectin-3 in the heart, cardiomyocyte apoptosis assays and gut microbiota analysis were detected. Left ventricular end-diastolic volume and diameter (LVVd and LVDd), and left ventricular end-systolic volume and diameter in the HF+SR group were significantly enlarged compared with those in the HF group (all P < 0.05). The HF+S group had a smaller LVDd and LVVd than the HF+SR group (5.01 ± 0.67 vs. 6.13 ± 0.45 mm, P = 0.033; 121.44 ± 38.74 vs. 189.94 ± 31.42 μL, P = 0.033). The messenger RNA and protein expression of galectin-3 and the number of apoptotic cardiomyocytes increased significantly in the HF+SR group compared to the HF group. Gut microbiota analysis showed that spermidine antagonists reduced the Firmicutes/Bacteroidetes ratio and changed the microbial community richness and diversity. In conclusion, spermidine can improve cardiac function in HF, and the regulation of gut microbiota and cardiac fibrosis may be a factor in the effect of spermidine on the improvement of cardiac function.Yufeng ChenZhiqin GuoShaonan LiShaonan LiZhen LiuZhen LiuPingan ChenFrontiers Media S.A.articleheart failurespermidinemicrobiotacardiac fibrosisgalectin-3Diseases of the circulatory (Cardiovascular) systemRC666-701ENFrontiers in Cardiovascular Medicine, Vol 8 (2021)
institution DOAJ
collection DOAJ
language EN
topic heart failure
spermidine
microbiota
cardiac fibrosis
galectin-3
Diseases of the circulatory (Cardiovascular) system
RC666-701
spellingShingle heart failure
spermidine
microbiota
cardiac fibrosis
galectin-3
Diseases of the circulatory (Cardiovascular) system
RC666-701
Yufeng Chen
Zhiqin Guo
Shaonan Li
Shaonan Li
Zhen Liu
Zhen Liu
Pingan Chen
Spermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-3
description Spermidine, which can be synthesized by the gut microbiota, can prevent cardiac hypertrophy and delay the progression to heart failure (HF). However, it is not clear whether the effect of spermidine on cardiac function is mediated by modulating the gut microbiota when HF occurs. Female HF Kunming mice induced by transverse aortic constriction were administered spermidine (HF+S group) or its antagonist (HF+SR group). Echocardiography, messenger ribonucleic acid (RNA) and protein expression of galectin-3 in the heart, cardiomyocyte apoptosis assays and gut microbiota analysis were detected. Left ventricular end-diastolic volume and diameter (LVVd and LVDd), and left ventricular end-systolic volume and diameter in the HF+SR group were significantly enlarged compared with those in the HF group (all P < 0.05). The HF+S group had a smaller LVDd and LVVd than the HF+SR group (5.01 ± 0.67 vs. 6.13 ± 0.45 mm, P = 0.033; 121.44 ± 38.74 vs. 189.94 ± 31.42 μL, P = 0.033). The messenger RNA and protein expression of galectin-3 and the number of apoptotic cardiomyocytes increased significantly in the HF+SR group compared to the HF group. Gut microbiota analysis showed that spermidine antagonists reduced the Firmicutes/Bacteroidetes ratio and changed the microbial community richness and diversity. In conclusion, spermidine can improve cardiac function in HF, and the regulation of gut microbiota and cardiac fibrosis may be a factor in the effect of spermidine on the improvement of cardiac function.
format article
author Yufeng Chen
Zhiqin Guo
Shaonan Li
Shaonan Li
Zhen Liu
Zhen Liu
Pingan Chen
author_facet Yufeng Chen
Zhiqin Guo
Shaonan Li
Shaonan Li
Zhen Liu
Zhen Liu
Pingan Chen
author_sort Yufeng Chen
title Spermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-3
title_short Spermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-3
title_full Spermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-3
title_fullStr Spermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-3
title_full_unstemmed Spermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-3
title_sort spermidine affects cardiac function in heart failure mice by influencing the gut microbiota and cardiac galectin-3
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/14d2dab2f2824d2592143a09aea413d7
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