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Purpose significance: pulmonary fibrosis caused by physical, chemical and biological factors, characterized by increased collagen deposition, clinical manifestations of progressive shortness of breath and even respiratory failure and death. So far, the molecular mechanisms remain elusive, no effective prevention and control measures. The development of pulmonary fibrosis species and individual differences, but the mechanism is yet to reveal the existence of such differences. Therefore, the subjects in the study C57BL/6J and the C3H/HeN mice RPI process differences based on the application of antibody microarray and tissue microarray technology to investigate the mechanism of their differences, look for pulmonary fibrosis prone molecules, and as the disease prevention a new target to further reveal the molecular mechanism of the disease and to explore and validate the prevention of new measures. Materials and methods: (1) 20Gy 60 Coγ ray irradiation C57BL/6J and C3H/HeN mice 30 each, after irradiation 1,3 and 6m, application HE and Sirius red staining, immune and tissue microarray detection Ⅰ and Ⅲ collagen expression, Hyp and argyrophilic protein content and FN, LN and α-SMA expression. (2) application of the the antibody microarray C57BL/6J and C3H/HeN mice before irradiation and the differences in protein expression in the the 3m lung tissue after irradiation. (3) in vitro culture mice LFs impose of 2,4,6 and 8Gyγ ray and 10 and 30nmol / L Rafl kinase inhibitor Ⅰ respectively at 6h after irradiation, 1, 2 and 3d applications MTT, flow cytometry and immunofluorescence cytochemistry method to detect cell viability, cell cycle, argyrophilic protein, α-SMA, MMP-1 and TIMP-1 expression. Experimental results: (1) in C57BL/6J mice after irradiation 1 ~ 6m lung histopathology changes experienced interstitial inflammation, cell proliferation and fibrosis stage 3 and 6m Ⅰ and Ⅲ collagen deposition and Hyp content significantly increased after irradiation, FN Rear 1 and 3m significantly higher, 6m reduce LN irradiated within 6m increased, α-SMA in 3 and 6m C3H/HeN mice after irradiation significantly increased; C3H/HeN mice irradiated 1 ~ 6m The lung tissue interstitial inflammatory changes, no collagen deposition Hyp content and FN 6m after irradiation, no significant changes in the irradiated, LN 1 ~ 3m significantly enhanced, 6m reduce. (2) preparation of radiation-induced lung damage tissue chip, HE staining and FN, LN and α-SMA immunohistochemical staining results with ordinary sections were stained with good consistency. (3) C3H/HeN mouse lung tissue before irradiation, high expression of DLP1, to shine upon 3m high to express MST3 and GSPT2; the C57BL/6J mice lung tissue after irradiation 3m express Rafl, TRF2 and HO1 high. (4) to 8Gyγ rays shine within 3d C57BL/6J and C3H/HeN mice LFs proliferation activity did not change. Aneuploidy C57BL/6J mice after irradiation LFs increased α-SMA high expression of MMP-1 expression was weakly positive, TIMP-1 expression was enhanced trend; 3d, see the C3H/HeN mice LFs after irradiation G 2 / M phase arrest, α-SMA expression was decreased MMP-1 and TIMP-1 expression showed an increasing trend. (5) Rafl kinase inhibitor Ⅰ role in C57BL/6J mice LFs after, α-SMA expression was decreased, and no non-aneuploid cells increased. Conclusions: (1) 20Gy 60 successful Coγ ray irradiation easy to establish / anti-radiation-induced lung fibrosis in animal models. C57BL/6J mice for easy fibrosis in mice, while C3H/HeN mouse antifibrotic mice. (2) the establishment of a radioactive lung injury Organization chip. (3) Rafl, TRF2 and HO1 with radiation-induced lung fibrosis was positively correlated, while MST3, and GSPT2 with the occurrence of radiation-induced lung fibrosis was negatively correlated. (4) C57BL/6J and C3H/HeN mice LFs, the different phenotypes, the functional activity of the state as well as irradiation of different reactivity, and both easy / anti pulmonary fibrosis. (5) Rafl kinase inhibitor Ⅰ can inhibit the the C57BL/6J mice LFs activity, a certain role in the prevention and treatment of RPF.
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