| 摘要: |
| 目的观察骨髓干细胞(BMSCs)动员后向栓塞肺组织归巢的情况,初步探讨BMSCs归巢栓塞肺组织的可能机制。方法选取30只健康的中国大耳白兔,雌雄不拘,随机分成2组: 肺血栓栓塞症(PTE)组(模型组)、PTE+粒细胞集落刺激因子(G-CSF)动员组(实验组),每组15只。经股静脉穿刺置管注入自体血栓,建立兔急性PTE模型。其中,模型组仅建立PTE模型;实验组在建立模型前4 d每天及建立模型后即刻按10 μg/(kg·d)皮下注射G-CSF,共5 d。两组均于建立模型后24 h处死动物,观察大体标本，行HE染色进行病理检查,用免疫组化法检测肺组织栓塞区、边缘区、正常区CD34及SDF-1的表达,使用医用图像处理系统对肺组织CD34和SDF-1的免疫组化染色切片进行图像分析,计算其相对含量。结果(1)大体标本观察: 两组兔肺组织均存在损伤性改变,表现为片状出血灶、局部肺组织苍白区、肺组织膨胀不全等。(2)光镜下病理观察: 两组兔肺组织栓塞区均表现为肺间质水肿充血、肺泡腔出血渗出,其中实验组栓塞区肺间质中可见较多体积较大的单个核细胞浸润。(3)肺组织CD34免疫组化染色与图像分析结果: CD34主要表达在栓塞区,边缘区少量表达,正常区很少表达。实验组栓塞区CD34的表达高于模型组(P<0.01),且实验组栓塞区内浸润的CD34阳性单个核细胞较多,而模型组少见。(4)肺组织SDF-1免疫组化染色与图像分析结果: SDF-1主要表达在栓塞区,边缘区、正常区均无表达。实验组栓塞区SDF-1的表达高于模型组(P<0.01)。结论PTE发生后存在CD34阳性BMSCs向栓塞肺组织归巢现象;PTE发生后肺组织栓塞区SDF-1表达加强可能是吸引CD34阳性BMSCs归巢栓塞肺组织的机制之一;使用G-CSF动员后能加强PTE后肺组织栓塞区SDF-1的表达,从而吸引更多的CD34阳性BMSCs归巢到栓塞肺组织。 |
| 关键词: 肺栓塞 粒细胞集落刺激因子 骨髓干细胞 归巢 基质细胞衍生因子1 CD34抗原 |
| DOI：10.3724/SP.J.1008.2012.001309 |
| 投稿时间：2012-09-27修订日期：2012-10-23 |
| 基金项目:南通市社会发展项目(S2008017). |
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| CD34+ bone marrow stem cells homing to embolized rabbit lung tissue |
| GU Jun1,NI Song-shi1*,HUANG Hua2 |
(1. Department of Respiratory Medicine, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China
2. Department of Pathology, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China
*Corresponding author.) |
| Abstract: |
| ObjectiveTo observe the homing of bone marrow stem cells (BMSCs) to the embolized lung tissues after mobilization and to investigate the potential mechanisms. MethodsThirty healthy Chinese big-ear rabbits were randomized into two groups regardless of gender: pulmonary thromboembolism (PTE) group (model group), PTE+granulocyte colony-stimulating factor (G-CSF) mobilization group (experimental group), with each group having 15 animals. Stable PTE models were established by injecting autologous thrombus into the femoral veins of the animals (model group). The animals in the experimental group received daily hypodermic injection of G-CSF (10 μg/\[kg·d\]) for five days, which was started 4 days before the establishing PTE models and ended at one day after the models were established. The animals were sacrificed 24 hours after modeling in both groups for general sample observation. Hematoxylin-eosin (HE) staining was done for the samples. Immunohistochemical analysis was done to detect the expressions of CD34 and SDF-1 in the embolized area, edge area, and normal area. A medical image processing software was used to analyze the results of immunohistochemical results to calculate the relative contents of CD34 and SDF-1. Results(1)General sample observation: the animals exhibited the damage of lung tissues in both groups, including splinter hemorrhage sites, local pale region and atelectasis. (2)Microscopic pathological observation: the embolized areas of all animals exhibited interstitial edema and hyperemia, and many red blood cells entered the pulmonary alveoli. Increased monocyte infiltration was detected in the experimental group. (3)Results of immunohistochemical analyses and image analyses of CD34: Most CD34 expression was found in the embolized area, very weak expression was found in the edge area, and hardly any was detected in the normal area. CD34 expression in embolized area was significantly higher in the experimental group than that in the model group (P<0.01). More monocytes expressing CD34 were seen in the experimental group and only a small number of them were found in the model group. (4) Results of immunohistochemical analyses and image analyses of SDF-1: Most SDF-1 expression was found in the embolized area, and no expression was found in the edge area and normal area. SDF-1 expression in embolized area was significantly higher in experimental group than in the model group (P<0.01). ConclusionBMSCs expressing CD34 can home to the embolized lung tissues after PTE. The increased SDF-1 expression may be one of the mechanisms of BMSCs homing to embolized lung tissues after PTE. Mobilization with G-CSF can increase SDF-1 expression in embolized area, which can attract more BMSCs to home to embolized lung tissues. |
| Key words: pulmonary embolism granulocyte colony-stimulating factor bone marrow stem cells homing stromal cell-derived factor-1 CD34 antigens |
