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在中年老鼠中,PM_2.5诱导的细胞衰老导致棕色脂肪组织受损

Renjie Hu¹, Wenjun Fan², Sanduo Li²

¹School of Public Health, Zhejiang Chinese Medical University, Hangzhou 310053, China; Zhejiang International Science and Technology Cooperation Base of Air Pollution and Health, Hangzhou 310053, China.

Ecotoxicology and environmental safety

|May 5, 2024

概括

空气中的细颗粒物 (PM2.5) 暴露会通过诱导细胞衰老和线粒体功能障碍,损害中年老鼠的棕色脂肪组织 (BAT). 这突显了年龄依赖于空气污染对代谢健康影响的脆弱性.

科学领域:

环境健康环境健康
代谢生理学代谢生理学
线粒体生物学线粒体生物学

背景情况:

空气中的细颗粒物 (PM2.5) 与代谢障碍有关,棕色脂肪组织 (BAT) 起着关键作用.
暴露于PM2.5对BAT功能的具体影响和潜在机制,特别是在不同的生命阶段,仍然不太清楚.

研究的目的:

研究PM2.5暴露对BAT表型和线粒体功能在不同年龄组小鼠中的影响.
阐明推动PM2.5诱导的BAT损害的分子机制,重点关注细胞衰老和相关途径.

主要方法:

暴露年轻,成年和中年老鼠于缩的环境PM2.5或过空气8周.
评估BAT形态 (H&E染色),线粒体功能 (高分辨率呼吸计) 和基因表达 (转录组学).
使用定量RT-PCR,免疫组织化学和免疫块进行转录组发现和机械探索的验证.

主要成果:

暴露于PM2.5引起了BAT形态和线粒体功能障碍的显著变化,特别是在中年老鼠中,在年轻或成年老鼠中没有明显的影响.
在中年老鼠中,PM2.5暴露导致BAT中细胞衰老的增加,其特征是细胞循环停止,DNA复制受损和AKT信号通路的抑制.
在中年老鼠的BAT中,暴露于PM2.5破坏了细胞亡和自的恒温,这表明了复杂的细胞反应.

结论:

与年轻年龄组相比,中年老鼠在BAT中对PM2.5暴露的脆弱性更高.
细胞衰老似乎是中年老鼠中PM2.5诱导的BAT损伤的关键发起因素,导致随后的亡,自干扰和线粒体功能障碍.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.自自是一种自的过程.棕色脂肪组织的脂肪组织.细胞衰老细胞衰老微细颗粒物质的细颗粒物质的细颗粒物质线粒体功能障碍线粒体功能障碍

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