中文摘要：

目的观察骨髓来源细胞（BMDCs）通过多途径在不同时间点参与肺损伤修复的作用。方法构建FVB/NJ小鼠博莱霉素诱导肺损伤模型,24 h或21 d后接受BMDCs或空培养基尾静脉注射,第7、14、21和28天取材,行HE染色、马森染色、羟脯氨酸含量检测和肿瘤细胞坏死因子-α（TNF-α）的Western blot检测。同时构建GFP骨髓嵌合小鼠模型,放射性肺损伤1个月后肺组织取材进行免疫荧光双标。结果早期输入BMDCs能明显缓解博莱霉素导致的肺组织炎细胞浸润和肺泡破坏等病理改变,降低各个时间点的羟脯氨酸含量至第21天达到最低值（P〈0.05）,在第7天明显下调肺内TNF-α的含量（P〈0.05）。推迟BMDCs输入的肺组织病理改变与对照组无差异。放射性肺损伤后1月,骨髓嵌合鼠中可见绿色荧光蛋白（GFP）与广谱细胞角蛋白（PCK）双阳性的BMDCs来源支气管上皮细胞和GFP与表面蛋白C（SPC）双阳性的BMDCs来源Ⅱ型肺泡上皮。结论早期输入BMDCs能通过多途径明显缓解放化疗引起的肺损伤。晚期输入BMDCs没有加重肺纤维化,对肺损伤也无缓解作用。

英文摘要：

Objective To observe the contribution of BMDCs to lung repair through multipath after lung injury.Methods FVB/NJ mice after bleomycin-induced lung injury received infusion of BMDCs 24 h or 21 d after lung injury.The mice were sacrificed at days 7,14,21,28,and HE stain,Martius Scarlet Blue stain,quantification of hydroxyproline and Western blot with TNF-α antibody were used.Meanwhile,a GFP chimeric mouse model was introduced to track BMDCs and induce irradiation lung injury,and immunofluorescent double labeling was carried one month after lung injury.Results Administration of BMDCs 24 h after lung injury attenuated the infiltrate of inflammatory cells and lesion of alveoli wall.The content of hydroxyproline in lung tissue decreased gradually and reached the lowest at days 21（P〈0.05）.TNF-α expression was suppressed at days 7（P〈0.05）.Administration of BMDCs 21 d after lung injury did not attenuate the histological damage.PCK＋/GFP＋ cells and SPC＋/GFP＋ cells were found in lung one month after irradiation.Conclusion Early administration of BMDCs could attenuate the lung injury induced by bleomycin and irradiation.Advantage or disadvantage of late administration were not observed.