The Research Of Prevention And Therapy Of Blood-activating And Stasis-dissipating Drugs In Radiation-induced Lung Injury

ObjectiveRadiation-induced lung injury (radiation pneumonitis and radiation pulmonary fibrosis) is a lung injury which normal lung tissues were radiated when radiotherapy was used in thoracic tumor. Its mechanism was complex. There were no effective prevention and treatment methods at present. The aim of the study was observed about pathological changes and expressions of transforming growth factor β (TGF-β) , tumor necrosis factor α (TNF-α) , interleukin 6 (IL-6 ) and fibroblast growth factor (FGF) in radiation-induced lung injury of rats in different radiation time by methods in pathology and molecular biology. And it was also observed about effects of blood-activating and stasis-dissipating drugs in expressions of above cell factors at the same time. And then it was discussed about the curative effect and the action mechanism of drugs. It would provide the theory basis for early prevention and treatment in radiation-reduced lung injury.Methods130 SD rats were randomly allocated into irradiation group (60 rats), treatment group (60 rats) and control group (10 rats). Animals in irradiation group and treatment group were radiated with x-rays in right lung at a dose of 3Gy after anesthesia twice weekly. The rats in treatment group started to be treated with blood-activating and stasis-dissipating drugs by gastrogavage oncedaily. The rats in irradiation group and control group were gavaged with 9% NS. And every 10 rats of irradiation group and control group were killed and specimens harvested on 1, 3, 5, 8, 12 and 26w after repeated irradiation respectively and counted lung coefficient. We observed the histological changes of their lungs stained with HE. And TNF-α, IL-6, TGF-β and bFGF were detected by immunohistochemistry.ResultsThe lung pathological change of rats in irradiation group was acute on early phase. It was remarkable in pulmonary edema, engorgement and hemorrhage. There was plenty of effusion in the pulmonary alveoli and inflammation cells soakage. The acute change became weaker and weaker from the twelfth week after the beginning of radiation and transformed into a subacute or chronic progressive phase. The pulmonary alveoli wall got seriously thick at late phase such as the twenty-sixth week after the beginning of radiation. Fibroblasts and fibrocytes reached a great number at that time. The weight of rats in irradiation group is less than control group ( P < 0.001 ). Treatment group didn't suffer from markedly pneumonia and pulmonary edema on early phase compared with irradiation group. And on late phase the level of fibrosis of treatment group was lighter than irradiation group.Expressions of TNF-a reached its peak at the fifth week ( P < 0.001 ) . the expression in treatment group was under irradiation group after the fourth week ( P < 0.001 ) . Expressions of IL-6 increased from the third to the twelfth week after the beginning of radiation and reached its peak at the eighth week ( P < 0.05 ). The expression was dim at the eighth week in treatment group( P < 0.01 ). Expression of TGF-β was high gradually in irradiation group, and got to its highest number at the twelfth week ( P < 0.001 ) . But its expression was dim in treatment group ( P < 0.001 ) . And the expression of bFGF was increased slowly to the highest at the twenty-sixth week, and its was higher than treatment group...