p38 MAPK通路在脂多糖致呼吸道上皮损伤中的作用

脂多糖（Lipopolysaccharide,LPS）是革兰阴性杆菌细胞壁的主要组成成分,也是一种很强的炎症反应和氧化应激诱导剂。呼吸道上皮是机体防御外界细菌、病毒、香烟烟雾等生物和化学因素损伤的天然屏障,在维持呼吸道局部微环境稳态中可发挥重要作用,也是吸入性药物治疗的主要靶细胞。呼吸道上皮结构完整性缺陷或功能紊乱还参与了哮喘、慢性阻塞性肺疾病等多种肺部疾病的发生和发展。LPS可引起呼吸道上皮损伤,但其具体的分子机制目前尚不清楚。p38丝裂原活化蛋白激酶（P38mitogen-activated protein kinase,p38 MAPK）作为MAPK家族四个亚家族成员之一,包含四个成员：p38α、p38β、p38γ和p38δ,可通过经典和非经典的p38 MAPK信号通路激活方式及通过激酶活性无关的功能参与调控炎症反应、细胞生长、细胞分化和细胞死亡等多种病理生理过程。本文就p38 MAPK信号通路在LPS致呼吸道上皮损伤中的作用做一综述。

Role of p38 MAPK Signal Pathway in Airway Epithelial Cells Injured by Lipopolysaccharide

Lipopolysaccharide（LPS）, one of the main components of the cell walls of Gram-negative bacteria, is one of the most important factors causing cell inflammation and oxidative stress. Airway epithelium is the body＇s natural defense barrier against the damage of biological and chemical factors such as bacteria, viruses and cigarette smoke, and plays the critical role in maintenance of homeostasis in the airway local microenvironment. Additionally, airway epithelium is the major target for the actions of a number of classes of inhaled medications, and dysfunction of homeostasis in airway epithelium structure or function may be involved in the pathophysiologic processes of many lung diseases such as asthma and chronic obstructive pulmonary disease. LPS can induce airway epithelial injuries, while the underlying molecular mechanism is still unclear. The p38 mitogen-activated protein kinase（p38 MAPK）including p38α, p38β, p38γ and p38δ, is one member lying within the four MAPK subfamilies, and it plays very important roles in regulating a wide variety of biological processes such as inflammation, cell growth, cell differentiation, and cell death, through classical or nonclassical p38 MAPK activation and independent of its kinase activity. This article reviews the role of p38 MAPK signal pathway in airway epithelial cells injured by lipopolysaccharide.