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首页> 外文期刊>International immunopharmacology >Protective effects of a neurokinin 1 receptor antagonist on airway epithelial mitochondria dysfunction in asthmatic mice via Nrf2/HO-1 activation
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Protective effects of a neurokinin 1 receptor antagonist on airway epithelial mitochondria dysfunction in asthmatic mice via Nrf2/HO-1 activation

机译:NEUROKININ 1受体拮抗剂对哮喘小鼠气道上皮线粒体功能障碍的保护作用,NRF2 / HO-1活化

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摘要

Bronchial asthma is a heterogeneous disease characterized by chronic airway inflammation with significant morbidity and mortality.Airway epithelial damage plays a crucial role in the pathogenesis of asthma [13]. The activation of airway epithelial cells can promote the Th2 immune response, secretion of a series of cytokines, and release of numerous inflammatory cells, such as eosinophils, lymphocytes, and macrophages. These inflammatory cells aggregate in the airways,wherein they are activated, causing further damage to the epithelium and release of a large amount of oxygen free radicals, causing oxidative stress [46]. Epithelial damage activates epithelial-mesenchymal repair, leading to airway remodeling [7,8], and mitochondria are the most important source of endogenous reactive oxygen species (ROS)[9]. The inhibition of mitochondrial damage, which in turn inhibits oxidative stress, is an effective method to reduce epithelial cell damage and inhibit airway remodeling and may be a new breakthrough strategy in asthma treatment [1012].
机译:支气管哮喘是一种异质性疾病,其特征在于慢性气道炎症,具有显着的发病率和死亡率。航道上皮损伤在哮喘发病机制中起着至关重要的作用[13]。气道上皮细胞的激活可以促进Th2免疫应答,分泌一系列细胞因子,并释放多种炎症细胞,例如嗜酸性粒细胞,淋巴细胞和巨噬细胞。这些炎症细胞在气道中聚集,其中它们被激活,导致对上皮的进一步损害并释放大量的氧自由基,从而引起氧化应激[46]。上皮损伤激活上皮 - 间充质修复,导致气道重塑[7,8],线粒体是内源性活性氧(ROS)最重要的来源[9]。抑制线粒体损伤,其又抑制氧化应激,是减少上皮细胞损伤和抑制气道重塑的有效方法,并且可能是哮喘治疗中的新突破性策略[1012]。

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