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肠道微生物组介导了心肌梗死后运动的保护作用。

Gut microbiome mediates the protective effects of exercise after myocardial infarction.

机构信息

Institute of Geriatrics (Shanghai University), (The Sixth People's Hospital of Nantong), School of Medicine, Affiliated Nantong Hospital of Shanghai University, Shanghai University, Nantong, 226011, China.

Cardiac Regeneration and Ageing Lab, School of Life Science, Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, Shanghai University, Shanghai, 200444, China.

出版信息

Microbiome. 2022 May 31;10(1):82. doi: 10.1186/s40168-022-01271-6.

Abstract

BACKGROUND

Gut microbiota plays important roles in health maintenance and diseases. Physical exercise has been demonstrated to be able to modulate gut microbiota. However, the potential role of gut microbiome in exercise protection to myocardial infarction (MI) remains unclear.

RESULTS

Here, we discovered exercise training ameliorated cardiac dysfunction and changed gut microbial richness and community structure post-MI. Moreover, gut microbiota pre-depletion abolished the protective effects of exercise training in MI mice. Furthermore, mice receiving microbiota transplants from exercised MI mice had better cardiac function compared to mice receiving microbiota transplants from non-exercised MI mice. Mechanistically, we analyzed metabolomics in fecal samples from exercised mice post-MI and identified 3-Hydroxyphenylacetic acid (3-HPA) and 4-Hydroxybenzoic acid (4-HBA), which could be applied individually to protect cardiac dysfunction post-MI and apoptosis through NRF2.

CONCLUSIONS

Together, our study provides new insights into the role of gut microbiome in exercise protection to MI, offers opportunities to modulate cardiovascular diseases by exercise, microbiome and gut microbiota-derived 3-HPA and 4-HBA. Video Abstract.

摘要

背景

肠道微生物群在维持健康和疾病方面发挥着重要作用。运动已被证明能够调节肠道微生物群。然而,肠道微生物组在运动对心肌梗死(MI)的保护作用中的潜在作用尚不清楚。

结果

在这里,我们发现运动训练改善了 MI 后心脏功能障碍,并改变了肠道微生物的丰富度和群落结构。此外,肠道微生物群的预先耗竭消除了运动训练对 MI 小鼠的保护作用。此外,接受来自运动 MI 小鼠的微生物移植的小鼠的心脏功能优于接受来自非运动 MI 小鼠的微生物移植的小鼠。从机制上分析了 MI 后运动小鼠粪便样本中的代谢组学,鉴定出 3-羟基苯乙酸(3-HPA)和 4-羟基苯甲酸(4-HBA),它们可以单独应用于保护 MI 后心脏功能障碍和通过 NRF2 诱导的细胞凋亡。

结论

总之,我们的研究为肠道微生物组在运动对 MI 的保护作用中的作用提供了新的见解,为通过运动、微生物组和肠道微生物组衍生的 3-HPA 和 4-HBA 调节心血管疾病提供了机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/673d/9153113/8f7489c194e2/40168_2022_1271_Fig1_HTML.jpg

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