32P-β 射线致急性放射性皮肤损伤模型的建立及损伤机制.

BACKGROUND: The clinical manifestation of acute radiation skin injury is recurrent necrotic ulcers, and its pathogenesis is still not fully understood. The establishment of a suitable animal model will have important clinical implications for the study of its pathogenesis, prevention and treatment. OBJECTIVE: To establish a model of acute β-ray radiation skin injury and to investigate the mechanism of injury. METHODS: Sixty-nine Sprague-Dawley rats were randomly divided into 30, 45, 60 Gy 32P-β-ray groups (n=21 per group) and control group (n=6). A single local irradiation of the back of the rats was performed using 32P radionuclide. The control group was operated in the same way as the irradiated groups except that it was not irradiated. The body mass and skin appearance of the rats were measured at 7, 15, 30, 45, and 60 days after irradiation. Three rats from each group were selected at each observation time point. The skin injury was observed by hematoxylin-eosin staining, Masson staining, transmission electron microscopy, and TUNEL assay. P53, Bcl-2 and Bax protein levels in the skin were measured by immunohistochemistry and western blot assay. RESULTS AND CONCLUSION: There was no accidental death after irradiation, and the body mass of rats showed a gradual increase. The rats showed different degrees of epidermal necrosis, inflammatory cell infiltration, reduction of hair follicles and appendages, and collagen fibrillation, which were evident at 60 and 45 Gy. The levels of serum inflammatory factors, interleukin-6 and tumor necrosis factor-α, were significantly increased in a dose-dependent manner. Under the electron microscope, there are varying degrees of mitochondrial reduction, vacuolization and nuclear pyknosis in the cells. The degree of cell apoptosis showed a certain dose-dependence. Immunohistochemistry and western blot results showed an increase in the expression of P53 and Bax proteins and a decrease in the expression of Bcl-2 protein in the skin after irradiation. There were significant differences between the 60 Gy group and the 45 Gy and 30 Gy groups (P < 0.05). To conclude, irradiation with 60 Gy and 45 Gy 32P radionuclide on the back of rats could successfully establish a practically pre-clinical animal model, and the mechanism is related to the up-regulation of P53 and Bax and the down-regulation of Bcl-2. This model can provide a reference for the establishment of animal models for the study of the mechanism of radiation skin injury and its prevention and treatment. [ABSTRACT FROM AUTHOR]