College of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, Changchun, 130000, People's Republic of China.
Graduate School, Beijing University of Chinese Medicine, Beijing, 100000, People's Republic of China.
Int J Chron Obstruct Pulmon Dis. 2022 Jul 12;17:1565-1575. doi: 10.2147/COPD.S366126. eCollection 2022.
Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis, emphysema, and small airway obstruction. Incompletely reversible airflow limitation, inflammation, excessive mucus secretion and bronchial mucosal epithelial lesions are the main pathological basis of the disease. The prevalence of COPD is increasingly worldwide, which has caused the burden on individuals and society. This paper summarizes the pathogenesis of COPD and clarifies the effect and mechanism of the latest targeted drugs for COPD. Besides, we focus on NOD-like receptor thermal protein domain associated protein 3 inflammasome (NLRP3 inflammasome). NLRP3 can promote production of interleukin-1β (IL-1β) and interleukin-18 (IL-18). NLRP3 is an important factor in the migratory aggregation of macrophages and neutrophils and the generation of oxidative stress. Inhibition of NLRP3 inflammasome indirectly blocks the inflammatory effects of IL-1β and IL-18, which may be regarded as an ideal target for COPD treatment.
慢性阻塞性肺疾病（COPD）包括慢性支气管炎、肺气肿和小气道阻塞。不完全可逆的气流受限、炎症、过度黏液分泌和支气管黏膜上皮损伤是疾病的主要病理基础。COPD 的患病率在全球范围内日益增加，给个人和社会带来了负担。本文总结了 COPD 的发病机制，阐明了 COPD 最新靶向药物的作用和机制。此外，我们还关注了 NOD 样受体热蛋白结构域相关蛋白 3 炎性小体（NLRP3 炎性小体）。NLRP3 可促进白细胞介素-1β（IL-1β）和白细胞介素-18（IL-18）的产生。NLRP3 是巨噬细胞和中性粒细胞迁移聚集以及氧化应激产生的重要因素。抑制 NLRP3 炎性小体可间接阻断 IL-1β 和 IL-18 的炎症作用，可能成为 COPD 治疗的理想靶点。
