抑制calprotectin可以减轻二氧化引起的肺纤维化
Narjes Saheb Sharif-Askari1,2, Bushra Mdkhana1, Shirin Hafezi1
1Research Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Inflammopharmacology
|May 17, 2025
概括
暴露会通过释放calprotectin (S100A8 / S100A9) 引起肺炎和纤维化. 用帕基尼莫德抑制calprotectin显示了对病和其他肺部疾病的治疗潜力.
科学领域:
- 免疫学 免疫学 免疫学
- 肺部病理学 肺部病理学
- 毒理学 毒理学 毒理学
背景情况:
- 呼吸的暴露会诱导肺部免疫病理和纤维化.
- 热蛋白蛋白 (S100A8/S100A9) 是由免疫细胞释放的,并且与慢性疾病中的纤维化有关.
- 对于calprotectin在病中的作用尚不完全了解.
研究的目的:
- 研究calprotectin在二氧化引起的肺纤维化中的作用.
- 评估帕基尼莫德作为治疗病的治疗剂.
主要方法:
- 化病小鼠模型来评估二氧化暴露的影响.
- 在体外研究中,使用使用S100A8/S100A9.9刺激的人类支气管纤维细胞进行了S100A8/S100A9.
- 对炎症标志物,纤维化指标 (EMT,原,MMP) 和NF-κB激活的分析.
- 用帕基尼莫德治疗以评估治疗疗效.
主要成果:
- 暴露增加了calprotectin,炎症和纤维化标志物 (EMT,原蛋白,MMPs).
- 在纤维细胞中S100A8/S100A9上调调节纤维菌标记物,被TLR4/RAGE抗剂和帕基尼莫德抑制.
- 帕基尼莫德治疗减少了肺病理,纤维化和NF-κB激活,使calprotectin水平正常化.
结论:
- 卡尔蛋白蛋白是症中炎症和纤维化的关键媒介.
- 帕基尼莫德证明了治疗气诱导的肺纤维化治疗的治疗潜力.
- 卡尔蛋白蛋白抑制为纤维炎性肺部疾病提供了一个有希望的策略.
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