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目的研究C57BL/6J小鼠双肺照射12Gy后,炎性细胞因子肿瘤坏死因子-α(TNF-α)、白介素-1α(IL-1α)和白介素-6(IL-6)蛋白在肺组织中的表达。方法实验组小鼠给予双肺单次照射12Gy,对照组小鼠在相同条件下双肺假照射0Gy。分别于照射后0·5、1、3、6、12、24、48和72h,1、2、4、8、16和24周处死,通过免疫组织化学方法和图像分析定量检测肺组织中TNF-α、IL-1α和IL-6蛋白的表达。结果胸部照射后数小时,上述炎性因子蛋白表达即比对照组显著增加。在随后的急性放射性肺炎阶段,支气管上皮以及肺间质的炎性细胞产生了大量的TNF-α(最大值出现在全肺照射后第4周,9·74%±1·78%)、IL-1α(最大值出现在全肺照射后第8周,14·76%±7·77%)和IL-6(最大值出现在全肺照射后第8周,4·28%±1·33%)。结论肺部照射以后,在胸部照射的最初数小时以内,支气管上皮是上述炎性因子最重要的来源,这些炎性细胞因子进一步通过征集和激活炎症细胞来促进和放大放射性肺炎的产生和发展。
Objective To investigate the expression of tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α) and interleukin-6 (IL-6) in pulmonary tissue of C57BL / expression. Methods Experimental mice were given a single lung irradiation 12Gy, control mice in the same conditions under the false lungs 0Gy. The mice were sacrificed at 0, 5, 1, 3, 6, 12, 24, 48 and 72h, 1, 2, 4, 8, 16 and 24 weeks after irradiation respectively. The levels of TNF in lung tissue were detected by immunohistochemistry and image analysis -α, IL-1α and IL-6 protein expression. Results Several hours after the chest irradiation, the expression of the above-mentioned inflammatory cytokines was significantly increased compared with the control group. During the subsequent stage of acute radiation pneumonitis, a large amount of TNF-α was produced in bronchial epithelial and interstitial inflammatory cells (maximum of 4.74% ± 1.78% at 4 weeks after whole lung irradiation), IL -1α (the maximum appeared in the eighth week after the whole lung irradiation, 14.76% ± 7.77%) and IL-6 (the maximum appeared in the eighth week after the whole lung irradiation, 4.28% ± 1.33 %). Conclusions After lung irradiation, bronchial epithelium is the most important source of these inflammatory factors within the first few hours of chest irradiation. These inflammatory cytokines further promote and amplify the production and development of radiation pneumonitis by collecting and activating inflammatory cells.