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来自肠道微生物群的丁酸盐可以通过GPR41防止大动脉剖析
Huan-Xin Yang1, Bing-Xin Wang1, Xiao-Liang Dong1
1MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Wuxi School of Medicine, Jiangnan University, Wuxi, 214122, China.
Acta pharmacologica Sinica
|June 23, 2025
概括
大动脉解剖 (AD) 是一种严重的疾病. 这项研究发现,补充肠道微生物代谢物丁酸盐,通过通过GPR41.1.改善血管光滑肌肉细胞功能来保护AD.
科学领域:
- 心血管研究研究心血管研究
- 微生物组研究 微生物组研究
- 代谢学 代谢学 代谢学
背景情况:
- 大动脉解剖 (AD) 是一种严重的疾病,其机制尚不清楚,治疗方法有限.
- 肠道微生物群及其代谢物在AD病变发生过程中的作用在很大程度上是未被探索的.
研究的目的:
- 调查肠道微生物群和丁酸盐对阿尔茨海默病发展的影响.
- 阐明丁酸盐在缓解AD进展方面的治疗潜力.
主要方法:
- 在小鼠中使用β-aminopropionitrile monofumarate (BAPN) 诱导的实验性AD.
- 在AD小鼠模型中分析了肠道微生物群组成和丁酸盐水平.
- 评估了外源性酸盐补充剂和淘汰赛小鼠模型 (GPR41,GPR109A) 的影响.
主要成果:
- 在AD小鼠中,肠道微生物群发生变化,产生酸盐的细菌减少,酸盐水平降低.
- 丁酸盐补充剂减弱了AD的进展,增强了血管光滑肌肉细胞收缩标志物.
- 丁酸盐抑制了NADPH氧化酶4的表达,减少了氧化应激和SMC表型切换.
- 丁酸盐的治疗效果取决于G蛋白结合受体41 (GPR41).
结论:
- 肠道微生物群失调和减少的丁酸盐都与AD病变发生有关.
- 外源性酸盐通过调节SMC功能和通过GPR41.1.减少氧化应激来显示AD的治疗潜力.
- 向肠道微生物群和丁酸盐代表了对大动脉剖析的有前途的治疗策略.
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