细胞自噬在哮喘肺气虚证中的作用机制及研究进展

Mechanism of Action and Research Progress of Autophagy in Asthma of Deficiency of Lung Qi Syndrome

支气管哮喘是一种由多种因素诱发的变态反应性疾病,是由多种细胞以及细胞组分参与的气道慢性炎症反应。而自噬作为一种蛋白质,脂类和细胞器溶酶体中降解的保守细胞进化过程。对气道炎症和肺纤维化中包括炎性细胞因子和炎症相关通路所导致的气道重塑都有重要影响。当哮喘日久,兼有肺气虚证后,随着肺气的功能减弱,气化不利,从而使得气血运行不畅,精、血、津液的生成、输布和代谢障碍以产生痰浊,会导致自噬基因Atg的表达降低与mTOR通路的活化,NF-κB信号通路过度激活,从而增加炎性因子的分泌、使得细胞程序性死亡,病理性产物过度积聚,导致哮喘进一步的加重。

Bronchial asthma is a kind of allergic disease induced by many factors.It is a chronic airway inflammatory reaction involving many kinds of cells and cell components.Autophagy,as a protein,evolves from the degradation of conserved cells in lipids and organelles lysosomes.It plays an important role in airway remodeling caused by inflammation and pulmonary fibrosis,including inflammatory cytokines and inflammatory related pathways.When asthma has a long term with lung Qi deficiency,with the function of lung Qi weakening and Qi movement being unfavorable,Qi and blood movement would be not smooth,the production,transportation and distribution disorder of essence,blood and body fluid could lead to phlegm,which will lead to the decrease of the expression of autophagy gene Atg and the activation of the mTOR pathway,and the excessive activation of the NF-κB signaling pathway,and thus increasing the secretion of inflammatory factors,programming cell death and excessive accumulation of pathological products and further leading to exacerbation of asthma.