鉴于放射性肺损伤是胸部肿瘤放疗的限制性因素，因此对其防护作用的研究一直是肿瘤放疗的热点。既往关于氧自由基损伤及炎性介质介导的观点仅能部分说明其发生机制，而放射性肺损伤后血管重建的机理及可能潜在的治疗靶点未得到足够的重视。本项目拟以通过单次20Gy一侧肺野照射的Wister大鼠为研究对象，建立放射性肺损伤模型，经过不同浓度的ACEI处理后，观察模型中肺内皮细胞，肺泡细胞的损伤程度以及其内CCL2的mRNA转录水平和蛋白质水平的变化，和由此被调控的肺巨噬细胞活化相关的NF-κB及Notch-1信号通路的改变；同时检测不同时相肺损伤模型局部组织及血清中炎性因子（TGF-β、IL-6、PGI2、TXA2、HP等）；评估模型动物肺血管重构的组织病理学、组织化学和血管动力学的变化等；力图阐明ACEI通过抑制肺血管重构而防治放射性肺损伤的机理，为ACEI防治放射性肺损伤提供可靠的依据。

Protection in radiation-induced pulmonary injury (RIPI) was becoming hot spot as results of RIPI regarded as an important dose-limiting toxicity during thoracic radiotherapy, and its pathogenesis was not clear due to pulmonary vascular remodeling tending to negligent, although oxygen free radical injury and inflammatory mediator definition were some good reasons for part. There, rat pulmonary injury models were established by a single dose of 20 Gy radiation to the right thorax, and exposed to different concentrations of angiotensin-converting enzyme inhibitor (ACEI) in different time phase, while as control. Injury of pulmonary vascular endothelium and pneumocyte was observed by morphology and immune-fluorescence staining, and chemokines in serum and cytokines in localized tissue (CCl2, TGF-β, IL-6, PGI2, TXA2,HP, et al) measured by RT-PCR, real time PCR or Western Bolting as well. Properly, NF-κB, Notch-1, the key of signal pathway related to activation of the alveolar macrophage, was assayed by knockout with anti-oligomers, while the correlation between alteration of NF-κB, Notch-1 and CCL2 probed. Finally, pulmonary vascular remodeling was evaluated by means of histopathology, immuno-histochemical staining, pathophysiology and hemodynamic change. it provides insight into strategies for protection with ACEI via the initial exploration of mechanism of pulmonary vascular remodeling in RIPI.