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PI3K/Akt-Nrf2 和大环内酯类药物在慢性阻塞性肺疾病中的抗炎作用。

PI3K/Akt-Nrf2 and Anti-Inflammation Effect of Macrolides in Chronic Obstructive Pulmonary Disease.

机构信息

Department of Respiratory and Critical Care Medicine, Liuzhou General Hospital, Liuzhou, Guangxi 545006, China.

Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China.

出版信息

Curr Drug Metab. 2019;20(4):301-304. doi: 10.2174/1389200220666190227224748.

DOI:10.2174/1389200220666190227224748
PMID:30827233
Abstract

BACKGROUND

Chronic Obstructive Pulmonary Disease (COPD) is a systematic inflammatory disease, and smoking is an important risk factor for COPD. Macrolide can reduce COPD inflammation. However, the inflammatory mechanism of COPD remains unclear and the anti-inflammatory mechanism of Macrolide is complex and not exactly known.

METHODS

We read and analysed thirty-eight articles, including original articles and reviews.

RESULTS

The expression of Nrf2 was lower in COPD patients and might have a protective role against apoptosis caused by CSE-induced oxidative stress. Nrf2 may play an important role in COPD inflammation. Nrf2 is a key factor in downstream of PI3K/Akt and is involved in the regulation of oxidative stress and inflammatory response. Therefore, PI3K/Akt pathway may play an important role in the activation of Nrf2 and COPD inflammation. Macrolide reduces lung and systemic inflammation of COPD by regulating PI3K/Akt pathway.

CONCLUSION

This review indicates that PI3K/Ak-Nrf2 may play an important role in COPD inflammation and macrolides may reduce lung and systemic inflammation of COPD by regulating PI3K/Akt-Nrf2 pathway. However, many crucial and essential questions remain to be answered. Further understanding of the mechanisms of macrolide efficacy and PI3K/Akt-Nrf2-mediated inflammatory responses may provide a new clue for exploring COPD treatment in the future.

摘要

背景

慢性阻塞性肺疾病(COPD)是一种系统性炎症性疾病,吸烟是 COPD 的重要危险因素。大环内酯类药物可以减轻 COPD 的炎症。然而,COPD 的炎症机制仍不清楚,大环内酯类药物的抗炎机制复杂,并不完全清楚。

方法

我们阅读和分析了 38 篇文章,包括原始文章和综述。

结果

COPD 患者 Nrf2 的表达水平较低,可能对 CSE 诱导的氧化应激引起的细胞凋亡具有保护作用。Nrf2 可能在 COPD 炎症中起重要作用。Nrf2 是 PI3K/Akt 下游的一个关键因素,参与氧化应激和炎症反应的调节。因此,PI3K/Akt 通路可能在 Nrf2 的激活和 COPD 炎症中起重要作用。大环内酯类药物通过调节 PI3K/Akt 通路减轻 COPD 的肺和全身炎症。

结论

本综述表明,PI3K/Akt-Nrf2 可能在 COPD 炎症中起重要作用,大环内酯类药物可能通过调节 PI3K/Akt-Nrf2 通路减轻 COPD 的肺和全身炎症。然而,仍有许多关键和重要的问题需要回答。进一步了解大环内酯类药物疗效的机制和 PI3K/Akt-Nrf2 介导的炎症反应,可能为未来探索 COPD 的治疗提供新的线索。

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