| ObjectiveRadiation therapy is the conventional treatment of thoracic cancer,70% of the esophageal cancer, non-small cell lung cancer need for radiotherapy. In an interview with irradiation, the lesions surrounding normal lung tissue will inevitably be exceeded its threshold of biological effects of radiation measurement, resulting in irreversible radiation damage (including radiation pneumonia and radiation-induced pulmonary fibrosis). A large number of clinical research and epidemiological investigations revealed that radiation-induced lung injury in patients with serious impact on the quality of life, and even may cause or hasten death. In particular, radiation-induced pulmonary fibrosis, a lack of effective modern medical treatment, but no method of early prevention and treatment. For the above reasons, this study was from a physiological point of view to conduct a preliminary study of the mechanism of radiation-induced lung injury,in hope to provide a basis for the treatment and prevention of that thoracic cancer radiotherapy and radiation side effects. A large number of experiments show that radiation-induced lung injury is involved in a variety of cells, a variety of cytokines in the complex process of regulation. Among them, the function of TGFβ1 is very broad,and it is known as the "switch" molecules and target molecules of treatment in the ccurrence and development of RPF.As all is well known,angiotensin II and aldosterone is an important part of the renin-angiotensin-aldosterone system (RAAS). Recent research found that, RAAS is also widespread in the heart, blood vessel wall, brain, lung, liver, kidney, adrenal glands and other tissues and organs, can cause heart,liver and renal interstitial fibrosis. Thus, angiotensinⅡ(AngⅡ)-aldosterone play a role in the radiation-induced lung injury and the causal relationship between TGF-β1 and angiotensin (AngⅡ)-aldosterone is the concern of this study.MethodsWistar rats were randomly divided into three groups, treatment groups were irradiated with 10MeV-βray linear accelerator at a dose of 16GY or 20 GY right hemi-thoracically.8 weeks after irradiation, TGF-β1 were detected with immunohistochemistry staining and ELISA, angiotensinⅡand aldosterone were detected by using ELISA, pathological change of lung tissues were stained with HE and Masson methods. SPSS 13.0 statisticl software was applied for statistical analysis. Data analysis using analysis of variance (LSD test),Differences were considered statistically significant at a value of P<0.05Resultsthere was statistical difference of the expression of TGF-β1 between non-irradiation group and irradiation groups, (P= 0.005,P<0.001), there was statistical difference between the two irradiation groups,P<0.001. Significant difference of expression level of angiotensinⅡwas seen between non-irradiation group and irradiation groups(P=0.021,P<0.001), there was statistical difference between the two irradiation groups, P=0.017.Compared with non-irradiation group, the aldosterone concentration of irradiation groups were higher(P=0.001,P<0.001). Significant difference was not detected between the two irradiation groups, P =0.131. Lung tissue inflammatory lesions and fibrosis were observed by HE and Masson stains in irradiation groups.Conclusion1.TGF-β1,AngiotensinⅡand aldosterone were highly expressed in radiation-induced lung injury, What's more, as the radiation doses rise, the level of its expression more significantly,and the relationship between radiation-induced lung injury more closely.2. There may be a certain relationship between the angiotensinⅡ-aldosterone and TGF-β13 TGF-β1,Angiotensin II and aldosterone plays an important pathophysiological role in the progress of radiation-induced lung injury.4. It may be desirable in the prevention and treatment of radiation-induced pulmonary injury to control synthesis or its role of angiotensinⅡ-aldosterone, TGF-β1...
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