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乳杆菌 Salivarius-Derived 印度尔-3-酸促进 AHR-PARP1 轴介导的 DNA 修复,以缓解肠道衰老

Zheng Cao^1,2, Cui Zhang^1,2, Hehua Lei^1,2

¹State Key Laboratory of Magnetic Resonance and Imaging, National Centre for Magnetic Resonance in Wuhan, Innovation Academy of Precision Measurement Science and Technology, Chinese Academy of Sciences (CAS), Wuhan, 430071, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|October 28, 2025

概括

亚利碳化合物受体 (AHR) 和多 (ADP-核糖) 聚合酶1 (PARP1) 轴缓解肠道衰老. 细菌的英多尔-3-酸 (IAA) 激活了AHR,增强了DNA修复和肠道功能.

科学领域:

老龄化和老年学
分子生物学分子生物学
微生物学微生物学

背景情况:

亚利碳化合物受体 (AHR) 和多 (ADP-ribose) 聚合酶1 (PARP1) 都与衰老有关.
连接AHR-PARP1轴与DNA修复在衰老中的机制尚不清楚.
老年人表现出肠道衰老,其特点是肠道失调,功能障碍和DNA损伤.

研究的目的:

为了研究AHR-PARP1轴在肠道衰老中的作用.
阐明AHR-PARP1信号影响DNA修复和肠道健康的机制.
确定潜在的治疗目标,以减轻与年龄相关的肠道功能障碍.

主要方法:

对年轻人和老年人和小鼠的肠道衰老进行比较分析.
调查英多尔-3-酸 (IAA) 对AHR激活和肠道衰老的影响.
涉及AHR-PARP1相互作用,PARylation和DNA损伤反应的机制研究.
在体内和体外实验,包括基因淘汰和淘汰模型.

主要成果:

老年人类和老鼠表现出显著的肠道衰老,肠道失生症和DNA损伤.
由细菌IAA激活肠道AHR通过调节DNA损伤反应来改善肠道衰老.
激活的AHR与PARP1相互作用,增强其活性并促进PARylation.
这个轴改善肠道屏障功能,减少炎症,抑制衰老.

结论:

AHR-PARP1轴在抵消肠道衰老方面发挥着至关重要的作用.
细菌IAA介导的AHR激活是缓解与年龄相关的肠道功能障碍的关键机制.
针对AHR-PARP1轴提供了针对与衰老相关的肠道疾病的干预的潜在策略.

关键词:

牛乳杆菌 (Lactobacillus salivarius) 是一种植物.亚利碳化合物受体 (AHR) 是一种印醇-3-乙酸的使用方法肠道衰老肠道衰老聚 (ADP-ribose) 聚合酶 1 (PARP1) 的使用情况.

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