摘要
Objective Radiation-induced lung injury (RILl) is the most common, dose-limiting complication in thoracic malignancy radiotherapy. Considering its negative impact on patients and restrictions to efficacy, the mechanism of RILl was studied. Methods Wistar rats were locally irradiated with a single dose of 0, 16, and 20 Gy to the right half of the lung to establish a lung injury model. Two and six months after irradiation, the right half of the rat lung tissue was removed, and the concentrations of TGF-[31, angiotensin II, and aldosterone were determined via enzyme-linked immunosorbent assay. Results Statistical differences were observed in the expression levels of angiotensin II and aldosterone between the non-irradiation and irradiation groups. Moreover, the expression level of the angiotensin II-aldosterone system increased with increasing doses, and the difference was still observed as time progressed. Conclusions Angiotensin II-aldosterone system has an important pathophysiological function in the progression of RILI.
Objective Radiation-induced lung injury(RILI) is the most common,dose-limiting complication in thoracic malignancy radiotherapy.Considering its negative impact on patients and restrictions to efficacy,the mechanism of RILI was studied. Methods Wistar rats were locally irradiated with a single dose of 0,16,and 20 Gy to the right half of the lung to establish a lung injury model.Two and six months after irradiation,the right half of the rat lung tissue was removed,and the concentrations of TGF-β1,angiotensinⅡ,and aldosterone were determined via enzyme-linked immunosorbent assay. Results Statistical differences were observed in the expression levels of angiotensinⅡand aldosterone between the non-irradiation and irradiation groups.Moreover,the expression level of the angiotensinⅡ-aldosterone system increased with increasing doses,and the difference was still observed as time progressed. Conclusions AngiotensinⅡ-aldosterone system has an important pathophysiological function in the progression of RILI.
基金
supported by grants from the National Natural Science Foundation of China(No.30900384)
Education Bureau Foundation of Liaoning Province,China (No.2009a723)