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目的观察小鼠放射性肺损伤过程中DNA损伤修复关键酶脱嘌呤/脱嘧啶核酸内切酶/氧化还原因子(apurinic/aprimidinic endonuclease/redox factor-1,APE1/Ref-1)表达的动态变化,初步探讨APE1/Ref-1在放射性肺损伤发生、发展中的作用。方法雌性昆明小鼠30只,随机分为照射组18只和对照组12只。照射组用8MV直线加速器给予小鼠全胸20Gy单次照射,对照组佯装照射。在照射后1、3、7、14、28、56d共6个时相点,分批活杀小鼠(照射组3只,对照组2只),观察其全肺大体形态改变,取右肺组织,光镜下观察组织形态学变化,免疫组化SP法检测APE1/Ref-1;取左肺组织,Western blot方法检测APE1/Ref-1蛋白表达。结果正常小鼠肺组织上皮细胞和内皮细胞中APE1/Ref-1呈胞核表达为主,而在小鼠放射性肺损伤不同阶段肺组织上皮细胞和内皮细胞中APE1/Ref-1表达特征有所改变,呈核浆共同表达和胞浆表达为主;并且APE1/Ref-1表达呈现先增高后降低的趋势,照射后1d开始升高,3d达高峰,且明显高于对照组,此后随着小鼠放射性肺损伤发展逐渐降低,28d降至对照组水平,56d明显低于对照组。结论电离辐射可以刺激APE1/Ref-1蛋白的表达并使其表达发生由核内转向浆内和先增高后降低的特征改变,表明APE1/Ref-1可能在放射性肺损伤修复过程中起着重要作用。
Objective To observe the dynamic changes of apurinic / aprimidinic endonuclease / redox factor-1 (APE1 / Ref-1), a key enzyme in DNA damage repair during radiation-induced lung injury in mice. To investigate the role of APE1 / Ref-1 in the occurrence and development of radiation-induced lung injury. Methods Thirty female Kunming mice were randomly divided into irradiation group (n = 18) and control group (n = 12). Irradiation group with a 8MV linear accelerator mouse full-chest 20Gy single irradiation, the control group pretend to irradiation. At 1, 3, 7, 14, 28, and 56 days after irradiation, 6 mice were sacrificed and the mice were sacrificed in batches (3 in irradiation group and 2 in control group). The general morphology of whole lung was observed. Histological changes were observed under light microscope. APE1 / Ref-1 was detected by immunohistochemical SP method. Left lung tissue and APE1 / Ref-1 protein expression were detected by Western blot. Results APE1 / Ref-1 was mainly expressed in epithelial cells and endothelial cells of normal mice. However, the expression of APE1 / Ref-1 in lung epithelial cells and endothelial cells was different at different stages of radiation-induced lung injury in mice The expression of APE1 / Ref-1 was first increased and then decreased, and then increased at 1 day and reached the peak at 3 days after irradiation, which was significantly higher than that of the control group The development of radiation-induced lung injury in mice decreased gradually, dropping to the level of the control group on the 28th day and significantly lower on the 56th day than that of the control group. Conclusion Ionizing radiation can stimulate the expression of APE1 / Ref-1 protein and change its expression from the nucleus to the first and then the decrease, indicating that APE1 / Ref-1 may play an important role in the repair of radiation-induced lung injury effect.