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氨基酸通过ROS/TXNIP/NLRP3途径加剧动脉样性血管炎症,这是一种有害的微生物代谢产物,由paeonol降低

Tian Wang¹, Hongfei Wu², Xiaoyan Shi²

¹Department of Pharmacy, Anhui University of Chinese Medicine, Hefei, Anhui 230012, China.

The international journal of biochemistry & cell biology

|November 4, 2024

概括

氨基酸 (AAA) 通过激活ROS/TXNIP/NLRP3通路,促进动脉样硬化 (AS) 的血管炎症. 醇 (Pae) 通过通过肠道微生物群来降低AAA水平来抑制AS,提供了一个新的治疗策略.

科学领域:

生物化学生化学
微生物学微生物学
心血管研究研究心血管研究

背景情况:

之前的一项研究确定了氨基酸 (AAA) 作为动脉样硬化 (AS) 小鼠中微生物的差异性代谢物,可疑是有害的.
AAA在促进AS血管炎症及其潜在机制中的确切作用仍然不清楚.
已知Paeonol (Pae) 有抗AS作用,但其对血清AAA水平的影响及其机制尚不清楚.

研究的目的:

调查氨基酸 (AAA) 是否促进AS血管炎症,并阐明其机制.
为了确定Paeonol (Pae) 是否通过降低血清AAA水平来发挥其抗风险效应.
探索肠道微生物群在Pae对AAA和AS的影响中的作用.

主要方法:

对AS患者血清AAA水平的临床分析与健康个体相比.
在体内研究中,使用AS小鼠补充了AAA或治疗了Pae.
在体外研究刺激人类静脉内皮细胞 (HUVECs) 用AAA.
评估大动脉斑块大小,脂质样本,炎症性细胞因子,氧化应激标志物 (ROS,马隆迪甲基) 和蛋白质水平 (ASC,TXNIP,NLRP3,caspase-1).
使用广谱抗生素和便微生物群移植进行微生物群操纵.

主要成果:

与健康对照组相比,AS患者的血清AAA水平较高.
AAA补充会加剧AS,增加斑块大小和炎症.
在HUVEC中AAA刺激增加了ROS并激活了NLRP3炎症酶途径,NAC和NLRP3抑制剂可以逆转效应.
在AS小鼠中,Pae治疗减少了AS斑块大小,改善了脂质配置文件,并减少了炎症.
在AS小鼠中,Pae通过肠道微生物群的传播降低了血清AAA水平,并抑制了大动脉NLRP3炎症酶的激活.
抗生素降低了Pae对NLRP3炎症酶的抑制作用.

结论:

氨基酸 (AAA) 通过激活ROS/TXNIP/NLRP3通路来促进AS血管炎症.
醇 (Pae) 通过降低血清AAA水平以微生物群依赖的方式抑制AS的发展.
AAA可以作为AS诊断的潜在生物标志物,Pae代表了AS的新治疗策略.

关键词:

氨基亚酸是一种氨基亚酸.动脉样硬化是一种动脉样硬化.微生物代谢物的微生物代谢物.这是一种Paeonol.血管内皮炎症血管内皮炎症

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