Abstract
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.
Highlights
Cardiac function and gut microbiota can affect each other
We investigated the effect of spermidine on heart failure (HF) by altering its levels and assessed the association between spermidine and gut microbiota in an HF model induced by transverse aortic constriction (TAC) to explore whether spermidine can affect cardiac function by modulating the gut microbiota
The results showed that the expression levels of spermidine were elevated in the HF+S group, and the relative protein expression levels of galectin-3 were higher in the HF+SR group than in the HF and HF+S groups (∼2.1-fold, all P < 0.05)
Summary
Cardiac function and gut microbiota can affect each other. Reduced cardiac output causes intestinal wall ischemia, edema and structural disruption of the intestinal epithelial barrier function in heart failure (HF), leading to increased intestinal permeability, which in turn, contributes to the progression of HF [1]. The impairment of intestinal barrier function leads to the translocation of gut bacterial deoxyribonucleic acid (DNA) and/or endotoxins into the bloodstream [2] and contributes to the deterioration of cardiac function [3]. Studies have shown that in chronic HF, the gut microbiota is characterized by large compositional shifts with low bacterial richness and depletion of the core microbiota [4, 5]. The intestinal microbiota plays an important role in the development and progression of HF [6,7,8].
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