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目的建立小鼠不同全身辐射剂量合并皮肤缺损模型,研究全身辐射对皮肤创面愈合的影响,探讨其病理生理学变化。方法采用180只雌性昆明种小鼠,60 Coγ射线一次性均匀照射4、6、8 Gy,照后30 min内,于小鼠背部制作1.5 cm×1.5 cm方形全层皮肤缺损伤口,构建不同全身放射剂量合并皮肤缺损动物模型(n=50),以单纯皮肤缺损作为对照组(n=30),各组动物于伤后3、5、7、10、14 d分别处死6只,取伤口全层皮肤组织,组织病理学检查伤口区炎细胞、成纤维细胞、新生毛细血管数量的变化;应用图像分析系统定量分析未愈伤口残余面积,统计14 d内各组动物存活率及体质量变化。结果 6 Gy放创组7 d和14 d的存活率分别为75%和55%,8 Gy放创组7 d时存活率仅33%,至10 d全部死亡。伤后14 d内,随辐射剂量的增加,放创组体质量较伤前降低程度愈加明显。全身辐射对皮肤创面愈合延迟随辐射剂量增加而加重:6、8Gy放创组2 d与对照组相比残余面积增大(P<0.01),4 Gy放创组伤后8 d与对照组相比残余面积增大,差异有统计学意义(P<0.05)。H-E染色显示:与对照组相比,放创组小鼠伤口早期炎症反应受抑,成纤维细胞和新生毛细血管数量增多明显滞后,肉芽组织形成延迟,上皮覆盖滞后。结论 6 Gy 60Coγ射线全身放射合并皮肤缺损伤的动物模型可为放创复合伤难愈机制的研究和早期的实验治疗提供研究平台。
OBJECTIVE: To establish a mouse model of skin defect with different whole body radiation doses and study the effect of whole body radiation on the healing of skin wounds and to explore the pathophysiological changes. Methods 180 female Kunming mice were irradiated with 4 Gy, 6 Gy and 8 Gy simultaneously with 60 Co γ ray. The full thickness 1.5 cm × 1.5 cm square full thickness skin defect was made on the back of the mice within 30 min after irradiation. Radiofrequency combined with skin defect animal model (n = 50), simple skin defect as a control group (n = 30), each group of animals were sacrificed 3, 5, 7, Layer of skin tissue, histopathological examination of wound area inflammatory cells, fibroblasts, capillary number of newborn changes; image analysis system for quantitative analysis of the callus residual area, statistics within 14 d of the survival rate and body weight of each group of animals. Results The survival rates of 7 Gy and 14 d were 75% and 55% in 6 Gy group and 33% in 7 Gy group and all the patients died in 10 days. Within 14 days after injury, with the increase of radiation dose, the quality of radiotherapy group decreased more obviously than that before injury. The delayed healing of the wound by the whole body radiation was aggravated with the increase of the radiation dose. The remnant area was increased in the 6 and 8 Gy groups (P <0.01) Than the residual area increased, the difference was statistically significant (P <0.05). H-E staining showed that compared with the control group, the inflammatory response of the wounds in the untreated group was inhibited at the early stage, the number of fibroblasts and neovascularization was obviously delayed, the formation of granulation tissue was delayed, and the epithelium covered lag. Conclusion The animal model of 6 Gy 60Co γ-ray combined with radiation-induced skin defect can provide a research platform for the research on the mechanism of refractory wound healing and the early experimental treatment.