肠道微生物群失生症与decabromodiphenyl以太诱导的骨质稳定性障碍有关,通过炎症引起的炎症
Ziyan Wang1, Wei Zhang2, Ziyan Liu2
1Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing, 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China.
Environmental pollution (Barking, Essex : 1987)
|January 21, 2025
概括
聚化二乙烯 (BDE-209) 暴露会通过改变肠道微生物群和促进炎症来破坏骨健康. 酸盐可能会减轻这些对骨质平衡的不良影响.
科学领域:
- 环境毒理学环境毒理学
- 骨生物学 骨生物学 骨生物学
- 微生物组研究 微生物组研究
背景情况:
- 与BDE-209一样,聚化二乙烯 (PBDE) 是环境污染物,与不良健康结果有关.
- 关于BDE-209对骨质稳定及其潜在机制的具体影响的研究是有限的.
研究的目的:
- 调查BDE-209暴露与骨健康之间的关系.
- 阐明涉及BDE-209对骨影响的机制,包括肠道微生物群和炎症.
- 为了评估甲酸盐的潜在缓解作用.
主要方法:
- 在体内研究中,使用雌性Sprague-Dawley大鼠暴露在BDE-209中60天,测量骨密度,微观结构,肠道微生物群和炎症标志物.
- 在体外研究中,使用THP-1细胞衍生的巨细胞,用BDE-209或甲酸盐治疗,以评估骨质细胞分化和炎症途径.
- 16s rRNA测序用于肠道微生物群分析.
主要成果:
- 暴露于BDE-209导致骨矿物质密度降低,骨质细胞活性增加和炎症性细胞因子 (IL-1β,TNF-α,IL-6) 的升高.
- 在BDE-209暴露的老鼠中观察到PGC-1α/NAD+/cGAS-STING通路的激活.
- 暴露于BDE-209改变了肠道微生物群的组成,减少了Lachnospiraceae的丰富性. 在体外,BDE-209通过cGAS-STING通路促进骨质细胞分化,这种效应被酸丁酸抑制.
结论:
- 暴露于BDE-209会通过肠道微生物群失调和炎症诱导骨质稳定性障碍.
- cGAS-STING通路和随后的炎症反应是BDE-209诱导的骨损伤的关键机制.
- 酸显示出作为治疗剂的潜力,可以抵消BDE-209对骨健康的有害影响.
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