CAJ | 학술논문

目的：利用放射诱导乳腺癌小鼠肺损伤，探讨放射诱导的肺损伤对乳腺癌小鼠实验性肺转移的影响。方法采用M A782细胞株建立小鼠乳腺癌模型。28只建模后的C57BL／6小鼠随机分为2组：对照组和照射组（每组 n＝14），右肺单次照射9 Gy后1～4周，观察记录其体重变化及肺、肝、脾等脏器转移情况；苏木精‐伊红（HE）染色观察肺组织形态学改变；免疫组化检测肺组织中趋化因子CXCL12／CXCR4的表达。结果照射后的1～2周，两组肝重、脾重和肺重变化无显著性差异（均 P＞0.05）；然而，随着照射时间的推移，照射组小鼠在3～4周肺重、肺结节和肺脏指数明显增加（ P＜0.05或 P＜0.01）。肺组织形态学观察显示，在照射后的早期（1～2周）出现炎性细胞浸润；在照射后的第3～4周出现更多的肺转移性结节；肺泡壁增厚明显，肺间质各种细胞成分增加；支气管壁及血管外膜有明显的纤维化增厚，肺泡区域有纤维化形成。照射组肺组织中CXCL12／CXCR4表达显著高于对照组。结论 X‐射线照射诱导的乳腺癌小鼠放射性肺损伤加速了肺转移，CXCL12‐CXCR4生物信号轴在肿瘤发展、侵袭和肺转移中发挥重要作用。
목적：이용방사유도유선암소서폐손상，탐토방사유도적폐손상대유선암소서실험성폐전이적영향。방법채용M A782세포주건립소서유선암모형。28지건모후적C57BL／6소서수궤분위2조：대조조화조사조（매조 n＝14），우폐단차조사9 Gy후1～4주，관찰기록기체중변화급폐、간、비등장기전이정황；소목정‐이홍（HE）염색관찰폐조직형태학개변；면역조화검측폐조직중추화인자CXCL12／CXCR4적표체。결과조사후적1～2주，량조간중、비중화폐중변화무현저성차이（균 P＞0.05）；연이，수착조사시간적추이，조사조소서재3～4주폐중、폐결절화폐장지수명현증가（ P＜0.05혹 P＜0.01）。폐조직형태학관찰현시，재조사후적조기（1～2주）출현염성세포침윤；재조사후적제3～4주출현경다적폐전이성결절；폐포벽증후명현，폐간질각충세포성분증가；지기관벽급혈관외막유명현적섬유화증후，폐포구역유섬유화형성。조사조폐조직중CXCL12／CXCR4표체현저고우대조조。결론 X‐사선조사유도적유선암소서방사성폐손상가속료폐전이，CXCL12‐CXCR4생물신호축재종류발전、침습화폐전이중발휘중요작용。
Objective To establish the radiation‐induced lung injury model in mice with breast cancer ,explore the effect of X‐ray irradiation on lung metastasis in these mice and observe whether the radiation‐induced lung injury will accelerate lung me‐tastasis.Methods The breast cancer model was established with MA782 cells in C57BL/6 mice by intraperitoneal injection.Twenty‐eight C57BL/6 mice after modeling were randomly divided into 2 groups:control group and irradiation group (n=14 in each group).In irradiation group ,the right chest was irradiated with a dose of 9 Gy one time when tumors grew to a‐bout 2 mm × 2 mm in diameter.One to four weeks after the irradiation ,the body weight was measured and liver ,lung and spleen metastases were observed.HE staining was used to observe the morphological changes of lung tissues and the expression of che‐mokine factor CXCL12/CXCR4 in lung tissues was immunohistochemically detected.Results There was no statistical signifi‐cance in the liver weight ,spleen weight and lung weight between the two groups 1 or 2 weeks after the irradiation(P>0.05) . With the irradiation time extended ,especially in 3-4 weeks ,lung weight ,lung nodules and lung index in the irradiation group were significantly increased(P<0.05 or P<0.01).Lung tissue morphology showed that the inflammatory cell infiltration was found in the early time(1-2 weeks)of irradiation;lung metastatic nodules were significantly increased 3-4 weeks after irradia‐tion;the alveolar wall was thickened and various cellular components in pulmonary interstitial tissues were obviously increased;fibrosis developed in the bronchial wall and vascular adventitia;fibrosis was found in the alveolar region.The expression level of CXCL12/CXCR4 was much higher in lung tissues in irradiation group than in control group.Conclusion X‐ray irradiation‐in‐duced lung radioactive injury accelerates lung metastasis in mice with breast cancer.CXCL12‐CXCR4 biological signal axis may play an important role in tumor development ,invasion and metastasis.