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首页> 外文期刊>Journal of cellular physiology. >Cholinergic anti-inflammatory pathway confers airway protection against oxidative damage and attenuates inflammation in an allergic asthma model
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Cholinergic anti-inflammatory pathway confers airway protection against oxidative damage and attenuates inflammation in an allergic asthma model

机译：胆碱能抗炎通路授予对氧化损伤和气道保护变弱在过敏哮喘炎症模型

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摘要

Asthma is characterized by the influx of inflammatory cells, especially of eosinophils as well as reactive oxygen species (ROS) production, driven by the release of the T helper 2 (Th2)-cell-associated cytokines. The cholinergic anti-inflammatory pathway (CAP) inhibit cytokines production and controls inflammation. Thus, we investigated the effects of pharmacological activation of CAP by neostigmine on oxidative stress and airway inflammation in an allergic asthma model. After the OVA challenge, mice were treated with neostigmine. We showed that CAP activation by neostigmine reduced the levels of pro-inflammatory cytokines (IL-4, IL-5, IL-13, IL-1β, and TNF-α), which resulted in a decrease of eosinophils influx. Furthermore, neostigmine also conferred airway protection against oxidative stress, attenuating ROS production through the increase of antioxidant defense, evidenced by the catalase (CAT) activity. We propose, for the first time, that pharmacological activation of the CAP can lead to new possibilities in the therapeutic management of allergic asthma.
机译：哮喘的特征是大量涌入的炎症细胞,特别是嗜酸性粒细胞和活性氧(ROS)生产,由辅助T 2的释放Th2细胞相关细胞因子。抗炎通路(CAP)抑制细胞因子生产和控制炎症。研究药物的影响激活新斯的明对氧化的帽子压力和过敏性气道炎症哮喘模型。用新斯的明治疗。激活新斯的明的水平降低促炎细胞因子(il - 4, IL-5 IL-13,il - 1β,TNF -α),导致下降嗜酸性粒细胞涌入。还授予气道保护氧化应激,衰减ROS生产通过抗氧化防御的增加,证明的过氧化氢酶(CAT)活性。首次提出,药理激活的帽子会导致新的治疗管理的可能性过敏性哮喘。

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