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分别采用流式细胞仪、细胞粘附实验和细胞粘附阻断实验，观察了单纯放射损伤（单放组）、单纯烧伤（单烧组）和放射复合伤（复合伤组）小鼠骨髓基质细胞表达细胞粘附分子（ＶＣＡＭ－１）、纤维连接素（Ｆｎ）、层粘素（Ｌｎ）和Ⅳ型胶原（ＣｏｌⅣ）的变化，以及基质细胞贴壁层对骨髓单个核细胞的粘附能力和对粒－单系造血祖细胞集落形成（ＧＭ－ＣＦＵ）能力的影响。结果：①骨髓基质细胞表达ＶＣＡＭ－１、Ｆｎ、Ｌｎ和ＣｏｌⅣ水平单烧组＞正常组＞复合伤组＞单放组；②基质细胞贴壁层对骨髓单个核细胞的粘附能力：伤后第３～７天，单烧组显著高于正常组（Ｐ＜０．０５～０．０１）、单放组低于正常组（Ｐ＜０．０５～０．０１）、复合伤组显著低于正常组（Ｐ＜０．０１）。提示，骨髓微环境基质细胞粘附功能的损伤可能是放射复合伤造血功能障碍发生的机制之一。
Flow cytometry, cell adhesion assay and cell adhesion inhibition test were used to observe the effects of radiation injury (single exposure group), simple burn injury (single burn injury) and radiation combined injury (multiple injury) mice bone marrow stromal The changes of cell adhesion molecule (VCAM-1), fibronectin (Fn), laminin (Ln) and collagen Ⅳ (Col Ⅳ) in cells and the adhesion of stromal cells to bone marrow mononuclear cells And on the ability of granulocyte-monophasic hematopoietic progenitor colony formation (GM-CFU). RESULTS: ① The levels of VCAM-1, Fn, Ln and ColⅣ in bone marrow stromal cells were significantly higher in single burn group> normal group> complex injury group than in single group. ② Adhesion of stromal cells to bone marrow mononuclear cells: From day 3 to day 7, the single burn group was significantly higher than the normal group (P <0.05 ~ 0.01), the single burn group was lower than the normal group (P <0.05 ~ 0.01), and the composite burn group was significantly lower In the normal group (P <0.01). It is suggested that the damage of bone marrow microenvironment stromal cell adhesion function may be one of the mechanisms of hematopoietic dysfunction in radiation combined injury.