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在慢性鼻炎的发病过程中APE1氧化还原功能的作用:针对性治疗的含义

Xiaojun Zhang¹, Jie Zhang², Changhua Wu³

¹Department of Otorhinolaryngology, Qilu Hospital of Shandong University, National Health Commission Key Laboratory of Otorhinolaryngology (Shandong University), Shandong Provincial Key Medical and Health Discipline of Qilu Hospital of Shandong University, Jinan, China; Department of Anesthesiology, Qilu Hospital of Shandong University, Jinan, China.

The Journal of allergy and clinical immunology

|July 19, 2025

概括

阿普里尼克/阿普里米尼克内核酶1 (APE1) 的氧化还原功能通过促进2型炎症和氧化应激,驱动带有鼻息肉的慢性鼻炎 (CRS). 用C10抑制APE1显示出治疗CRS的治疗潜力.

科学领域:

生物化学生物化学
免疫学免疫学免疫学
病理生理学病理生理学

背景情况:

阿普里尼克/阿普里米尼克内核酶1 (APE1) 具有内核酶和氧化还原功能.
APE1的氧化还原活性会影响参与细胞存活,血管生成和炎症的转录因子.
在具有鼻息肉的慢性鼻炎 (CRS) 中APE1氧化还原功能的特定作用尚不清楚.

研究的目的:

研究APE1氧化还原函数在CRS发展中的作用.
评估针对CRS治疗的氧化还原抑制剂对APE1的治疗潜力.

主要方法:

在人类鼻腔组织中分析了APE1的表达和功能,使用包括单细胞RNA测序,免疫组织化学,西斑和qRT-PCR在内的技术.
使用了CRS小鼠模型,空气-液体接口培养的人类鼻上皮细胞和BEAS-2B细胞.
研究了APE1氧化还原抑制剂 (C10) 对2型免疫反应,粘液高分泌,上皮屏障完整性和氧化应激的影响.

主要成果:

在CRS中增加的APE1表达与鼻息肉相关,与乙酸的透,粘液过分分泌,上皮损伤和氧化应激有关.
用C10抑制APE1氧化还原功能的药理学抑制减少了细胞中的IL-25产量,并减少了小鼠和细胞模型中的2型细胞因子 (IL-4,IL-5,IL-13) 和免疫细胞透.
准APE1减轻了反应性氧物种的产生,氧化应激和线粒体损伤.

结论:

APE1的氧化还原功能在CRS病理生理学中起着重要作用,有助于2型炎症,氧化应激,粘液产生和上皮屏障功能障碍.
APE1氧化还原抑制剂C10有效抑制了2型炎症并改善了CRS病理.
针对APE1氧化还原功能的治疗是CRS治疗的有前途的治疗策略.

关键词:

在APE1中,APE1是APE1.这是一种APE1氧化还原抑制剂.C1010 一个人的心态它们是IL-25和IL-25.慢性犀牛鼻炎慢性鼻炎氧化应激障碍是一种氧化应激障碍.状细胞的细胞.这是一种2型炎症.

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