Mechanism Of Pulmonary Tissue Remodeling In Early Radiation Lung Injury

Objective: To explore the mechanism of pulmonary tissue remodeling and reveal the relationship among alveolar macrophage, fibroblast, collagen IV (Col IV) and gelatinase B in early radiation pulmonary injury (RPI). Methods: The lungs of mice and rats were irradiated by ⁶⁰Co γ ray. General RNA was extracted from mouse lungs. The condition medium of alveolar macrophage (CMAM) was prepared by using rat lung lavage. The role of CMAM promoting human lung fibroblast (HLF) proliferation was measured by MTT. The increase of Col IV and activity of gelatinase B were detected by western blot and zymography respectively, and illustration analysis was performed. The expression of Col IV and gelatinase B gene in mice lungs was determined by RT-PCR.Results: CMAM could significantly promoted HLF proliferation. Synthesis of Col IV in HLF was markedly increased at 6h, 12h and decreased at 24h after administration of CMAM. The activity of gelatinase B was increased at 24h, and kept in a high level at 48h and then it was decreased at 72h. The RNA transcription of Col IV was increased gradually from 1w to 4w, and that of gelatinase B was increased at lw and then began to decrease at 2w after irradiation in mice. Conclusions: Incidence of radiation pulmonary fibrosis (RPF) may be related to the disbalance between Col IV and gelatiase B during remodeling of lungs tissue in early radiation pulmonary injury.