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目的:探讨构建血管内皮细胞持续分泌炎症因子的血管损伤模型的方法。方法:2 Gy分割剂量的6 MV-X线(2Gy/F,5F/W,总计40Gy)照射人脐静脉融合细胞系EA. Hy926,照射野35cm×35cm,源皮距100cm。在照射期间及末次照射后1月,2月,3月,4月,5月提取细胞总RNA、总蛋白,以未照射组为对照组,采用实时荧光定量RT-PCR方法检测炎症相关因子转录水平表达情况,Western Blot法检测炎症因子蛋白水平的表达情况。结果:经2Gy×20次放疗后1-5月,人脐静脉融合细胞系EA. Hy926细胞炎症因子,与对照组相比,在转录与蛋白水平,表达均升高(P<0.05)。结论:放射性血管损伤细胞模型中,内皮细胞EA. Hy926炎症因子表达上调,导致放疗后血管损伤,促进放疗后晚期皮肤纤维化的发生。
OBJECTIVE: To explore a method for establishing a vascular injury model in which vascular endothelial cells continuously secrete inflammatory factors. Methods: The human umbilical vein fusion cell line EA9.1 Hy926 was irradiated with 2 Gy dose of 6 MV-X (2Gy / F, 5F / W, total 40 Gy). The irradiation field was 35 cm × 35 cm and the source skin was 100 cm. Total RNA and total protein of cells were extracted during the irradiation and the last irradiation in January, February, March, April and May, and the non-irradiated group was used as the control group. Real-time fluorescent quantitative RT-PCR was used to detect the transcription of inflammatory related factors The level of expression, Western Blot assay inflammatory protein expression levels. Results: Inflammatory cytokines in human umbilical vein endothelial cells (EA-Hy926) cells were significantly increased at transcription and protein levels (P <0.05) compared with the control group from January to May after 2Gy × 20 radiotherapy. Conclusion: The expression of inflammatory factor EA. Hy926 in endothelial cells is up-regulated in the radiation-induced vascular injury cell model, leading to vascular injury after radiotherapy and promoting the occurrence of advanced fibrosis after radiotherapy.