放射性肺损伤(RILI)发生机制比较复杂,目前最为公认“细胞因子级联”学说，其中电离辐射引起的氧化应激是炎症微环境形成、免疫失衡引起后续级联效应的始动因素。氧化应激损伤引起自噬活性的改变，自噬作为一种保护机制，能减轻氧化损伤、促进细胞生存，因此RILI与自噬存在一定的相关性。AMPK是生物体内普遍存在的一种丝氨酸/苏氨酸蛋白激酶，通过直接和间接方式激活诱导自噬，AMPK的激活可以抑制TNF-α、IL-1β、IL-6的表达。前期研究证实中药“养阴清肺活血”法治疗 RILI 可有效减轻放射性肺炎肺组织炎症程度，降低TGF-β、IL-6、TNF-α的表达与释放。所以本课题通过研究体外肺实质细胞以及体内肺组织在辐射后局部存在氧化损伤和自噬现象，探讨AMPK介导自噬的发生机制；通过“养阴清肺活血法”干预,初步探讨其通过AMPK调控自噬在RILI的作用，为中药新药开发应用提供新的理论依据。

The mechanism of radiation-induced lung injury (RILI) is complex. According to cytokine cascade theory,the most widely accepted mechanism recently, oxidative stress induced by ionizing radiation is the initiating factor for subsequent cascade effect, caused by the formation of inflammatory micro-environment and the immune imbalance. Oxidative stress damage can induce the change of the autophagy activity. Whereas, autophagy, as a protective mechanism, can reduce oxidative damage and promote cell survival.Therefore,there is a certain relevance between RILI and autophagy. AMPK, an ubiquitous serine / threonine protein kinase in organism, could be activated directly or indirectly and then induce autophagy. The activation of AMPK can inhibit TNF-α, IL-1 β, IL-6 expression through direct and indirect activation induced autophagy. Early studies have confirmed that "Yangyinqingfeihuoxue" therapy in Chinese medicine could effectively reduce the degree of radioactive pneumonia lung tissue inflammation and the expression and release of TGF -β, IL-6, TNF-α.In this study, we will discuss the mechanism of autophagy induced by AMPK activation through observing the local oxidative damage and autophagy in lung parenchymal cells and lung tissue in vivo after radiation. By using "Yangyinqingfeihuoxue" therapy, initially discuss the role of autophagy induced by AMPK in RILI and provide new theoretical basis for the development and application of new Chinese medicine.