过高homocysteinaemia通过抑制Nrf2/HO-1信号通路而加剧牙周炎
Kaiqiang Yang1,2,3,4, Yuting Yang1,2,3,4, Ting Long1,2,3,4
1Center of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People's Republic of China.
Redox report : communications in free radical research
|March 10, 2025
概括
超同胞蛋白血症 (HHcy) 通过增加炎症和骨质损失使牙周炎恶化. 这通过高氧化应激和抑制Nrf2/HO-1信号发生,影响骨质细胞活动.
科学领域:
- 口腔生物学 口腔生物学
- 生物化学 生化学
- 病理学 病理学 病理学
背景情况:
- 牙周炎会引起炎症和骨质损失,导致牙损失.
- 超同胞蛋白血症 (HHcy) 与心血管疾病和潜在的牙周炎有关.
- 连接HHcy和牙周炎进展的机制尚未完全理解.
研究的目的:
- 为了研究HHcy如何加剧牙周组织炎症.
- 探索HHcy在牙周炎骨质细胞形成中的作用.
- 阐明涉及HHcy诱导牙周炎的分子途径.
主要方法:
- 使用一种带有HHcy诱导的牙周炎动物模型.
- 检查了牙组织中的炎症标志物和蛋白质表达.
- 在使用LPS/Hcy和Rankl/Hcy.治疗的RAW264.7细胞和骨质细胞中研究了细胞反应.
- 评估了活性氧物种 (ROS) 和Nrf2/HO-1信号通路活性.
主要成果:
- HHcy加剧了牙周连接损失和增加了全身/牙炎症.
- 抗氧化蛋白被抑制,而氧化损伤标志物在HHcy模型中增加.
- 在LPS刺激细胞中,HHcy提高了ROS水平,并抑制了Nrf2/HO-1通路.
- HHcy抑制了Nrf2/HO-1信号传递,增加了骨质细胞标记物 (NFATc-1,CTSK),并增强了骨质细胞生成.
结论:
- HHcy通过增加氧化应激和炎症而加剧牙周炎症.
- Nrf2/HO-1信号通路在调解HHcy的有害影响方面发挥着至关重要的作用.
- HHcy促进骨质细胞的产生,有助于牙周炎的骨质损失.
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