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PM2.5 通过 AhR 介导的氧化应激诱导心肌细胞衰老

Tiantian Liu¹, Bin Jiang², Baoqiang Fu¹

¹School of Biology and Basic Medic Sciences, Suzhou Medical College, Soochow University, Suzhou 215123, China.

Antioxidants (Basel, Switzerland)

|July 27, 2024

概括

颗粒物 (PM2.5) 暴露会通过激活基碳水化合物受体 (AhR) 和增加氧化应激,导致心脏细胞衰老. 准这种AhR/ROS通路可能会防止PM2.5诱导的心脏衰老.

科学领域:

环境健康环境健康
心血管生物学心血管生物学
细胞衰老细胞衰老

背景情况:

暴露于PM2.5与心血管疾病有关,但其对心肌细胞衰老的影响尚不清楚.
之前的研究集中在血管衰老,留下关于心脏细胞衰老的知识差距.
了解PM2.5对心脏细胞的影响对于公众健康至关重要.

研究的目的:

研究PM2.5可提取有机物 (EOM) 对心肌细胞衰老的影响.
阐明PM2.5诱导的心脏衰老背后的分子机制.
探索减轻PM2.5引起的心脏衰老的潜在治疗点.

主要方法:

H9c2心肌细胞暴露于PM2.5 EOM.
评估了细胞衰老标志物 (β-银酸酶,p16,p21,H3K9me3).
测量了细胞循环进展,活性氧物种 (ROS),DNA损伤和酸受体 (AhR) 路径激活.

主要成果:

PM2.5 EOM诱导了细胞衰老,细胞循环停止 (G1/S),并增加了ROS和DNA损伤.
抗氧化剂N-乙半氨酸 (NAC) 和AhR抗剂CH223191减弱了EOM诱导的衰老.
EOM暴露激活了AhR通路,表明它在PM2.5的影响中的作用.

结论:

暴露于PM2.5通过AhR激活促进心脏衰老,导致氧化应激,DNA损伤和细胞循环停止.
AhR/ROS轴是PM2.5诱导的心脏衰老的一个关键调解器.
准AhR/ROS通路是针对PM2.5相关心脏衰老的潜在治疗策略.

关键词:

啊啊啊啊啊啊啊啊啊啊啊啊啊啊啊啊啊啊啊啊在PM2.5中,PM2.5是最常见的.心肌细胞的细胞是心肌细胞.氧化应激是一种氧化应激.衰老是一种老化.

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