大细胞迁移抑制因子可能会在阻塞性睡眠呼吸暂停中促进氧化的产生
Risaki Kawachi1,2, Yoshiki Kobayashi1,2, Hisashi Ooka1,3
1Department of Otorhinolaryngology-Head and Neck Surgery, Kansai Medical University, Hirakata, Japan.
Journal of sleep research
|September 8, 2025
概括
持续的正气压 (CPAP) 疗法通过减少巨细胞迁移抑制因子 (MIF) 和相关的炎症来改善阻塞性睡眠呼吸暂停 (OSA) 的鼻氧化 (NO).
科学领域:
- 呼吸系统医学 呼吸系统医学
- 免疫学 免疫学 免疫学
- 睡眠医学 睡眠医学
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 涉及反复阻塞呼吸道,导致粘膜炎症和增加鼻氧化 (NO) 生产.
- 导致OSA患者NO升高的确切机制尚不完全理解.
研究的目的:
- 研究阻塞性睡眠呼吸暂停 (OSA) 患者鼻腔中氧化物 (NO) 生产升高的潜在机制.
- 评估持续正气道压力 (CPAP) 治疗对OSA患者局部鼻炎和NO水平的影响.
主要方法:
- 在八名中度至重度OSA患者的CPAP治疗前后测量了鼻氧化 (NO) 水平.
- 分析鼻粘膜上浮体中的炎症性细胞因子和上皮细胞中炎症相关分子的mRNA表达.
- 在体外刺激呼吸道上皮细胞,使用鼻膜上浮体和复合性巨细胞迁移抑制因子 (MIF).
主要成果:
- CPAP疗法显著降低了鼻腔NO水平,并在鼻腔粘膜中降低了巨细胞迁移抑制因子 (MIF).
- 在CPAP治疗后,鼻上上皮细胞中SIRT1mRNA表达增加,HIF-1α和可诱导氧化合成酶 (iNOS) mRNA表达减少.
- 大细胞迁移抑制因子 (MIF) 对气道上皮细胞的刺激导致SIRT1的减少和HIF-1α和iNOS表达的增加.
结论:
- 患有OSA患者鼻腔粘膜的局部炎症变化与NO的产量增加有关,其中巨细胞迁移抑制因子 (MIF) 发挥着潜在的作用.
- 持续的正气道压力 (CPAP) 治疗有效调节这些炎症通路,降低OSA患者的NO水平和炎症.
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