在巨细胞中,NAT10通过NOX2-ROS-NF-κB通路调节LPS诱导的炎症反应
Zhanqi Zhang1, Yiwen Zhang1, Yongjie Cai1
1Hospital of Stomatology, Sun Yat-sen University, Guangzhou 510055, China; Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou 510055, China; Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou 510055, China.
Biochimica et biophysica acta. Molecular cell research
|June 12, 2023
概括
N-乙转移酶10 (NAT10) 通过激活巨细胞中的NOX2-ROS-NF-κB通路来加速牙周炎炎症. 它的抑制剂雷莫德林 (Remodelin) 通过减少炎症和骨质损失,显示出治疗牙周炎的潜力.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 牙周病学 牙周病学
背景情况:
- 牙周炎是一种慢性炎症性疾病,涉及巨细胞.
- N-乙转移酶10 (NAT10) 调节炎症反应.
- 目前尚不清楚NAT10在牙周炎病原体中的作用.
研究的目的:
- 研究NAT10在牙周炎中巨介导炎症中的作用.
- 阐明NAT10影响牙周炎症的分子机制.
- 评估NAT10抑制在牙周炎中的治疗潜力.
主要方法:
- 在LPS诱导的炎症中评估NAT10表达.
- 在巨细胞中利用了NAT10的淘汰和过度表达.
- 进行RNA测序以确定受影响的途径.
- 研究了NF-κB信号传递和活性氧物种 (ROS) 的作用.
- 评估了NAT10抑制在牙周炎小鼠模型中的作用.
主要成果:
- 在LPS诱导的炎症中,NAT10表达减少.
- NAT10调节的炎症因子生成和NF-κB信号传递.
- NAT10促进了ROS生成,并提高了Nox2表达的调节.
- 在体内,NAT10抑制减少了巨细胞的透和骨再吸收.
结论:
- NAT10通过NOX2-ROS-NF-κB通路加速巨细胞中LPS诱导的炎症.
- 用雷莫德林抑制NAT10表明了牙周炎的治疗潜力.
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