醇-3-化物通过AhR/Nrf2信号通路保护牙上皮膜屏障结构和功能
Lingzhi Wu1,2,3, Shiwen Wu1,2,3, Yuquan Deng1,2,3
1Hospital of Stomatology, Sun Yat-Sen University, No. 56, Lingyuan West Road, Guangzhou, Guangdong, 510055, China.
Inflammation
|January 7, 2026
概括
印醇-3-化物 (IAld) 通过通过酸受体 (AhR) 和Nrf2通路加强牙上皮屏障,防止牙周炎,减少炎症和骨质损失.
科学领域:
- 口腔生物学 口腔生物学
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 牙周炎涉及慢性炎症和上皮质屏障功能障碍.
- 众所周知,甲基的代谢物英多尔-3-化物 (IAld) 通过基碳水化合物受体 (AhR) 改善表皮屏障.
研究的目的:
- 通过AhR激活来研究IAld在保护牙周炎的牙上皮质中的作用和机制.
- 评估IAld对牙周炎的治疗潜力.
主要方法:
- 建立了牙周炎的小鼠模型,采用微型CT,组织学和16S rRNA测序分析.
- 使用了用P. gingivalis刺激的人类牙上皮细胞 (hGECs) 的体外试验 (CCK-8,FITC-FD4流量,西式涂抹,免疫光).
- 进行RNA测序,免疫光和免疫组织化学,以探索分子机制.
主要成果:
- 在牙周炎小鼠的IAld治疗减少了膜骨损失,牙周炎症,并激活了AhR通路.
- 增加了紧结蛋白表达 (E-cadherin,Claudin1,Occludin,ZO-1) 和调节了口腔微生物群.
- 在体外,IAld降低了hGEC的透性,上调了CYP1A1,E-cadherin和Claudin1,减少了ROS的产生,并增强了Nrf2/HO-1抗氧化途径.
结论:
- 在牙周炎中,IAld保留了牙上皮质屏障的完整性和功能.
- 保护机制涉及AhR/Nrf2信号通路的激活和抗氧化剂反应.
- IAld提出了一种有前途的治疗策略,用于治疗牙周炎.
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