论文部分内容阅读
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4d每天及建立模型后即刻按10μg/(kg·d)皮下注射G-CSF,共5d。两组均于建立模型后24h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。
Objective To observe the homing of embolized lung tissue after mobilization of bone marrow stem cells (BMSCs), and to explore the possible mechanism of BMSCs homing to pulmonary embolism. Methods Thirty healthy Chinese white rabbits were randomly divided into two groups: pulmonary thromboembolism (PTE) group (model group), PTE + G-CSF mobilization group (experimental group) , Each group of 15. Autologous thrombus was injected into femoral vein catheter to establish rabbit acute PTE model. In the model group, only PTE model was established. In the experimental group, G-CSF was injected subcutaneously at 10μg / (kg · d) every day 4 days before the model was established and immediately after establishing the model, for 5 days. Animals were sacrificed 24 hours after the model was established. Gross specimens were examined for pathological examination by HE staining. Expressions of CD34 and SDF-1 in the embolic area, marginal area and normal area of lung tissue were detected by immunohistochemistry. The system of lung tissue CD34 and SDF-1 immunohistochemical staining sections were image analysis, calculate the relative content. Results (1) Gross specimen observation: Both groups of rabbits showed damage of lung injury, manifested as flaky hemorrhage, local pale area of lung tissue, lung tissue dilatation and so on. (2) Pathological observation under light microscopy: Both groups of pulmonary embolism showed pulmonary interstitial edema congestion, alveolar hemorrhage exudation, in which the experimental group of pulmonary embolism seen more bulky mononuclear cells infiltration. (3) Immunohistochemical staining and image analysis of CD34 in lung tissue: The expression of CD34 mainly in the embolic area, a small amount in the marginal zone and few in the normal area. The expression of CD34 in the experimental group was higher than that in the model group (P <0.01), and there were more CD34 positive mononuclear cells in the experimental group than in the model group. (4) The results of immunohistochemical staining and image analysis of SDF-1 in lung tissue: The main expression of SDF-1 in the embolic area, marginal area and normal area showed no expression. The expression of SDF-1 in the experimental group was higher than that in the model group (P <0.01). CONCLUSIONS: The presence of CD34-positive BMSCs into the embolized lung tissue after PTE occured. The enhanced expression of SDF-1 in the pulmonary embolism area after PTE may be one of the mechanisms that may attract the homing of CD34-positive BMSCs to pulmonary embolism. After G-CSF mobilization Can enhance the expression of SDF-1 in the pulmonary embolism area after PTE, thereby attracting more CD34-positive BMSCs to homing to the embolized lung tissue.