摘要
目的:放射性肺损伤是一种常见的、与放射剂量相关的胸部恶性肿瘤放疗并发症,考虑到对患者严重的不良反应及对治疗的限制,本实验初步探讨了放射性肺损伤的发生机制。方法:雌性Wistar大鼠57只,随机分成三组(每组19只):对照组(2组),照射16 Gy组(2组),照射20 Gy组(2组),右肺予不同照射剂量(0、16、20 Gy)。2或6个月后,取大鼠右肺组织,ELISA方法检测肺组织中TGF-β1、血管紧张素Ⅱ、醛固酮含量。结果:对照组与照射组比较,大鼠肺组织血管紧张素Ⅱ、醛固酮的表达均有统计学差异,并且具有放射剂量和时间的依赖性。结论:初步研究结果显示血管紧张素Ⅱ-醛固酮系统在放射性肺损伤的发生发展过程中具有重要的作用,但机制需要进一步研究证明。
Objective： Radiation-induced lung injury （RILI） is the most comon, dose-limiting complication in thoracic malignan- cy radiotherapy. Considering its negative impact on patients and restrictions to efficacy, the mechanism of RILI was studied. Methods： In this experiment, Wistar rats were locally irradiated with a single dose of 0, 16, or 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, angiotensin Ⅱ, and aldosterone were determined via enzyme-linked immunosorbent assay. Results： Statistical differences were bserved 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. Conclusion： Our preliminary results demonstrate that the angiotensin Ⅱ-aldosterone system has an important patho- physiological function in the progression of RILI. However, further studies should be done to determine the mechanism of this progres- sion.
出处
《中国肿瘤临床》
CAS
CSCD
北大核心
2013年第5期253-256,共4页
Chinese Journal of Clinical Oncology
