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.

亚精胺可以由肠道微生物群合成，可以预防心脏肥大并延缓向心力衰竭 (HF) 的进展。然而，尚不清楚亚精胺对心脏功能的影响是否是通过在发生 HF 时调节肠道微生物群来介导的。将亚精胺（HF+S 组）或其拮抗剂（HF+SR 组）给药于由横向主动脉缩窄诱导的雌性 HF 昆明小鼠。检测超声心动图、信使核糖核酸 (RNA) 和心脏中 galectin-3 的蛋白质表达、心肌细胞凋亡测定和肠道微生物群分析。HF+SR组左心室舒张末期容积和直径（LVVd和LVDd）、左室收缩末期容积和直径均较HF组明显增大（所有磷< 0.05)。HF+S 组的 LVDd 和 LVVd 小于 HF+SR 组（5.01 ± 0.67 对 6.13 ± 0.45 mm，磷= 0.033; 121.44 ± 38.74 与 189.94 ± 31.42 μL，磷= 0.033）。与HF组相比，HF+SR组galectin-3的信使RNA和蛋白表达以及凋亡心肌细胞数量显着增加。肠道微生物群分析表明亚精胺拮抗剂降低了厚壁菌门/拟杆菌门比例并改变了微生物群落的丰富度和多样性。综上所述，亚精胺可以改善心衰患者的心功能，肠道菌群的调节和心脏纤维化可能是亚精胺改善心功能的一个因素。