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作 者:陈幸华[1,2,3] 罗成基[1,2,3] 郭朝华[1,2,3] 王苹 邓学才[1,2,3]
机构地区:[1]第三军医大学附属新桥医院全军肿瘤中心 [2]第三军医大学全军复合伤研究所 [3]第三军医大学基础部
出 处:《中华放射医学与防护杂志》1999年第3期186-190,共5页Chinese Journal of Radiological Medicine and Protection
基 金:全军"八五"攻关基金
摘 要:目的初步探讨放射复合伤对骨髓造血微环境中基质细胞粘附功能损伤的机理。方法采用流式细胞仪、细胞粘附实验和细胞粘附阻断实验等方法,检测50Gyγ射线全身照射、15%体表面积Ⅲ度烧伤和放射复合伤小鼠骨髓基质细胞表达血管细胞粘附分子(VCAM1)、纤维连接素(Fn)、层粘素(Ln)和Ⅳ型胶原(ColⅣ)等成分的变化以及骨髓基质细胞贴壁层对骨髓单个核细胞粘附能力的影响。结果①骨髓基质细胞表达VCAM1、Fn、Ln和ColⅣ的水平具有以单烧组>正常组>复合伤组>单放组的特点。②伤后第3~7天,单烧组骨髓基质细胞的粘附能力显著高于正常组(P<005~P<001);单放组和伤后第3天的复合伤组则反之。③分别用VCAM1、Fn、Ln和ColⅣ单抗处理骨髓基质细胞贴壁层后,骨髓单个核细胞的粘附率较未加单抗组均有不同程度的下降。结论骨髓微环境基质细胞粘附功能的损伤可能是影响放射复合伤骨髓造血功能障碍的原因之一。Objective\ To investigate the adherent function of bone marrow stromal cells in hematopoietic inducive microenvironment post combined radiation burn injury. Methods The expression of cell adhesion molecules including vascular cell adhesion molecule 1(VCAM 1),fibronection(Fn),laminin (Ln) and collagen type IV (Col Ⅳ) on bone marrow stromal cells cultured in vitro was detected by flow cytometry and the binding capacity of bone marrow mononuclear cells to stromal cell adherence layer was tested by cell binding assay and cell binding blocking assay respectively from mice treated with 5.0 Gy γ ray 15% of total body surface area (TBSA),third degree burn injury and combined irradiation burn injury,respectively. Results 1.The expression levels of molecules mentioned above in burn injured mice were the highest.The molecules levels in control mice were greater than those in radiation injured mice,which were lower than those in mice with combined radiation burn injury.2.The binding capacity of stromal cell adherence layer in burn injured mice was greater than that in control mice,and significantly increased from 3 to 7 days post injury as compared with that in controls,radiation injured mice and combined radiation burn injured mice, respectively ( P <0 05-0 01).Contrarily,the capacity of binding in the radiation injured and combined radiation burn injured mice was the lowest from 3 to 7 days post injury.3.The binding rate of bone marrow mononuclear cells to stromal cell adherence layer descended in different degrees after pre treatment with monoclonal antibodies directed to VCAM 1,Fn,Ln,or Col Ⅳ respectively or VCAM 1 combined with anti Fn,anti Ln or anti Col Ⅳ,respectively,in stromal cell adherence layer. Conclusion The damage of cell adherent function for bone marrow hematopoietic inducive microenvironment post combined radiation burn injury might be one of the important factors in hematopoietic disorder in combined radiation burn injury.
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