酸/FBP1通过肠心轴参与聚乙烯纳米塑料诱导的心脏损伤
Huiwen Kang1, Danyang Huang1, Wei Zhang1
1Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, 10 Xitoutiao, You An Men, Beijing, 100069, China.
Particle and fibre toxicology
|May 9, 2025
概括
微/纳米塑料 (MNPLs) 暴露会破坏肠心轴,从而损害心脏功能. MNPLs降低酸水平,抑制FBP1的表达,导致心脏毒性.
科学领域:
- 环境毒理学环境毒理学
- 心血管研究研究心血管研究
- 微生物组研究 微生物组研究
背景情况:
- 微/纳米塑料 (MNPLs) 是普遍存在的环境污染物,具有已知的有毒作用.
- MNPL诱导的心脏毒性的具体机制,特别是通过肠心轴,仍然不清楚.
研究的目的:
- 研究聚烯纳米塑料 (PS-NP) 对心脏功能的影响.
- 阐明肠心轴及其代谢物在PS-NP诱导的心脏毒性的作用.
主要方法:
- 人类心肌细胞 (AC16) 和心脏组织暴露于80nmPS-NP.
- 使用16S rRNA测序对肠道微生物群和短链脂肪酸 (SCFA) 的分析.
- 心脏和结肠组织的转录组分析.
- 在体外干预使用 propionate 和 FBP1 激活剂 (BML-275).
主要成果:
- PS-NP 导致心脏功能受损,心肌原沉积增加.
- PS-NPs改变了肠道微生物群的组成,并降低了酸水平.
- 减少酸与心脏和结肠组织中果糖-1,6-双酸酶1 (FBP1) 的表达减少有关.
- 在体外实验证实了酸的保护作用和FBP1的参与.
结论:
- 肠心轴在纳米塑料诱导的心脏毒性中发挥着关键作用.
- 由于MNPL暴露而降低的酸水平抑制了FBP1的表达,损害了心脏功能.
- 这些发现确定了减轻纳米塑料诱导心脏损伤的潜在治疗点.
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