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目的探讨当归注射液对辐射损伤小鼠骨髓有核细胞黏附分子表达及增殖周期的影响。方法BALB/c小鼠随机分为3组:正常组、照射组和当归注射液预防组。正常组:即未经照射组。照射组:于照射前3d起给予10ml·kg-1·d-1无菌生理盐水腹腔注射。当归注射液预防组:于照射前3d起给予腹腔注射当归注射液2·5g·kg-1·d-1。于照射后第7天断颈处死小鼠,取出股骨,计数骨髓单个核细胞。经流式细胞仪分别检测骨髓单个核细胞黏附分子CD49d和CD49e及G0/G1期细胞百分率和周期蛋白D2表达水平。结果与正常组比较,照射组造血细胞明显减少,骨髓有核细胞黏附分子CD49d和CD49e表达明显下降,G0/G1期细胞百分率明显增加,而细胞周期蛋白D2表达水平明显降低,当归注射液预防组能增加骨髓单个核细胞计数,明显提高细胞黏附分子CD49d和CD49e的表达,降低G0/G1期细胞百分率,提高细胞周期蛋白D2的表达水平。结论当归注射液能通过提高细胞黏附分子表达水平,刺激细胞周期蛋白D2的表达促进造血细胞的增殖。
Objective To investigate the effects of Angelica sinensis injection on bone marrow nucleated cell adhesion molecule expression and proliferation cycle in irradiated mice. Methods BALB/c mice were randomly divided into 3 groups: normal group, irradiation group and Angelica Injection prevention group. Normal group: the non-irradiated group. Irradiation group: 10 ml·kg-1·d-1 sterile saline was intraperitoneally injected 3 days before irradiation. Angelica injection prevention group: given 3 days before irradiation, intraperitoneal injection of Angelica injection 2. 5g · kg-1 · d-1. On the 7th day after irradiation, the mice were killed by cervical dislocation, the femurs were removed, and bone marrow mononuclear cells were counted. The percentages of CD49d, CD49e and G0/G1 phase cells and cyclin D2 expression in bone marrow mononuclear cells were detected by flow cytometry. Results Compared with the normal group, hematopoietic cells in the irradiated group were significantly decreased, the expression of CD49d and CD49e in bone marrow nucleated cells was significantly decreased, the percentage of cells in the G0/G1 phase was significantly increased, and the expression level of cyclin D2 was significantly decreased, and the Danggui injection group was prevented. It can increase the bone marrow mononuclear cell count, significantly increase the expression of cell adhesion molecules CD49d and CD49e, reduce the percentage of G0/G1 phase cells, and increase the expression of cyclin D2. Conclusion Danggui injection can promote the proliferation of hematopoietic cells by increasing the expression level of cell adhesion molecules and stimulating the expression of cyclin D2.