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间歇性禁食通过肠道代谢物英多尔-3- propionate 抑制血小板激活和血栓形成

Zhiyong Qi^1,2, Luning Zhou^1,2, Shimo Dai^1,2

¹Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, 180 Fenglin Road, Shanghai 200032, China.

Life metabolism

|March 13, 2025

概括

间歇性禁食 (IF) 降低了血小板激活和血栓形成风险. 这种效应是由产生英多尔-3-酸 (IPA) 的肠道细菌调节的,该酸准血小板PXR信号通路.

科学领域:

心血管研究研究心血管研究
代谢健康代谢健康
微生物组研究微生物组研究

背景情况:

血小板过敏反应是发生心脏病发作和中风等血栓事件的关键因素.
目前的抗血小板疗法留下了剩余的缺血风险.
间歇性禁食 (IF) 对血小板激活的影响尚不清楚.

研究的目的:

为了研究IF对血小板激活和血栓形成的影响.
阐明IF对血小板的作用的基本机制.
评估IF在缓解缺血症/再输液损伤方面的潜力.

主要方法:

研究了IF对冠状动脉疾病患者和阿波利波蛋白E淘汰赛小鼠的血小板激活的影响.
分析了肠道微生物群和英多尔-3-酸 (IPA) 在IF影响中的作用.
研究了IPA在血小板信号传递中的分子标,包括孕前X受体 (PXR) 和下游途径.

主要成果:

间歇性禁食在人类患者和动物模型中显著抑制了血小板激活和血栓形成.
如果肠道菌群增加了英多尔-3-酸 (IPA) 的产量.
升高的IPA通过与血小板PXR结合直接降低了血小板激活,抑制了Src/Lyn/Syk和LAT/PLCγ/PKC/Ca2+信号传递.
在小鼠中,IF治疗缓解了心肌和脑缺血/再输血损伤.

结论:

间歇性禁食减轻了冠状动脉样硬化中的血小板激活和血栓形成风险.
增强肠道微生物IPA的产生是IF抗血小板作用的关键调解者.
IPA激活血小板PXR信号通路为减少血栓形成风险提供了一个新的治疗点.

关键词:

在PXR中,PXR就是PXR.动脉血栓形成动脉血栓形成印醇-3- propionate 的使用方法断断续续的禁食是一种禁食.血小板激活是什么意思

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