老化肠道微生物群通过氧化应激促进心律失常的易感性
Zhi-Ping Fu1, Yi-Ge Ying1, Rui-Yao Wang1
1Collage of Pharmacology, North China University of Science and Technology, Tangshan 063200, China.
iScience
|October 9, 2024
概括
老龄化改变了肠道微生物群,增加了心律失常的风险. 这项研究表明,老化的肠道微生物通过氧化应激传递心律失常的易感性,影响离子通道.
科学领域:
- 心脏病学 心脏病学
- 微生物学 微生物学
- 老年学是一门学科.
背景情况:
- 心律失常和突然心脏死亡 (SCD) 是重大的健康负担,患病率随着年龄的增长而增加.
- 肠道失调症越来越被认为是导致与年龄有关的疾病,包括心律不整的因素.
研究的目的:
- 研究老化肠道微生物群在促进心律失常的因果作用.
- 阐明关联肠道微生物群,氧化应激和衰老中的心律失常的潜在机制.
主要方法:
- 从老年小鼠移植便微生物群 (FMT) 给年轻小鼠,以评估心律失常的易感性.
- 在老年小鼠中使用抗生素消耗肠道微生物群.
- 研究氧化应激标记物和离子通道蛋白质表达.
- 肠道微生物群代谢物的移植和Vitexin的使用.
主要成果:
- 心律不整的易感性是通过FMT从老年小鼠传染给年轻小鼠的.
- 在老年小鼠中,肠道活性氧物种 (ROS) 的增加与减少的离子通道蛋白表达和心律失常相关.
- 抗生素诱导的肠道微生物群枯竭减少了老年小鼠的ROS和心律失常.
- 老化肠道微生物群在年轻小鼠中诱导了氧化应激,而Vitexin通过OLA1-Nrf2通路减轻了衰老和心律失常.
结论:
- 衰老的肠道微生物群通过诱导全身氧化应激来促进心律失常,从而降低心脏离子通道蛋白表达.
- 针对肠道微生物群和氧化应激通路,为与年龄有关的心律失常提供了潜在的治疗策略.
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