Chronic obstructive pulmonary disease (COPD) is a chronic and devastating condition characterized by poor airflow and breath. Smoking and other environmental factors–caused inflammations triggered excessive autophagy of normal lung epithelial cells, eventually leading to impaired lung functions. Previous studies showed that ghrelin exhibited beneficial effects on patients with COPD. However, the mechanisms underlying this impact remained largely unknown. In this study, in vitro and in vivo models of COPD‐associated inflammation were established, and we found that inflammation and autophagy were abonormally activated through nuclear factor kappa b (NF‐κB) and activator protein‐1 (AP‐1) signaling pathways. Interestingly, ghrelin could inhibit the excessive inflammation pathways and autophagy induced by particle matter and/or cigarette extract in bronchial epithelial cells. Furthermore, NF‐κB and AP‐1 signaling were both inhibited while lung functions were significantly improved. Taken together, identification of downstream signaling of ghrelin in inflammation provided a new avenue in the treatment of COPD.

中文翻译：

---

Ghrelin可改善慢性阻塞性肺疾病相关的炎症和自噬

慢性阻塞性肺疾病（COPD）是一种慢性破坏性疾病，其特征是气流和呼吸不良。吸烟和其他环境因素引起的炎症引发正常肺上皮细胞过度自噬，最终导致肺功能受损。以前的研究表明，生长素释放肽对COPD患者显示出有益的作用。但是，造成这种影响的机制在很大程度上仍然未知。在这项研究中，体外和体内建立了COPD相关炎症模型，我们发现炎症和自噬是通过核因子κB（NF-κB）和激活蛋白-1（AP-1）信号通路异常激活的。有趣的是，生长素释放肽可以抑制支气管上皮细胞中的颗粒物和/或香烟提取物诱导的过度炎症途径和自噬。此外，NF-κB和AP-1信号均被抑制，而肺功能得到明显改善。两者合计，在炎症中生长素释放肽的下游信号的鉴定提供了治疗COPD的新途径。