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目的 探讨放射损伤后巨噬细胞对血细胞生成的负性调节作用。方法 昆明种雄性小鼠经 6Gy6 0 Coγ射线一次性全身照射后 ,检测辐照后 1、3、7、15d腹腔巨噬细胞 (PCMΦ)数量和吞噬墨汁的能力 ;用ELISA和放免法检测巨噬细胞培养上清TGF β1 、MIP 1α和TNFα的含量 ;将不同数量的巨噬细胞加入骨髓有核细胞中 ,观察其对CFU E和CFU GM形成的影响 ;骨髓有核细胞剔除Mac 1+ 细胞及再加入不同比例的巨噬细胞后对CFU E和CFU GM形成的影响。结果 ①放射损伤后巨噬细胞吞噬功能增强 ;培养上清TNFα、TGF β1 和MIP 1α水平升高 ;经LPS刺激后放射损伤组巨噬细胞培养上清此 3种因子的水平无显著改变。②骨髓细胞中当加入 10 %以上正常巨噬细胞时生成的CFU E和CFU GM数量明显减少 ,当加入相同比例的放射损伤巨噬细胞生成的CFU E和CFU GM数量减少更加显著。③剔除Mac 1+ 细胞后的骨髓细胞生成CFU E和CFU GM数量增加 ,当再加回巨噬细胞数量又减少。结论 放射损伤后巨噬细胞被激活 ,造血抑制活性增强 ,这可能是放射损伤骨髓造血功能受抑的原因之一。
Objective To investigate the negative regulatory effect of macrophages on hematopoiesis after radiation injury. Methods Kunming male mice were exposed to 6Gy 60Coγ-rays for 1 whole body irradiation. The number of peritoneal macrophages (PCMΦ) and phagocytosis of ink were detected at 1, 3, 7 and 15 days after irradiation. The macrophages were detected by ELISA and radioimmunoassay The contents of TGFβ1, MIP 1α and TNFα in cell culture supernatant were determined. Different numbers of macrophages were added to bone marrow nucleated cells to observe the effect on CFU E and CFU GM formation. Macrophages were excised Mac 1+ cells and The effects of different ratios of macrophages on the formation of CFU E and CFU GM were also investigated. Results ① The phagocytosis of macrophages was enhanced after radiation injury. The levels of TNFα, TGFβ1 and MIP 1α in the culture supernatant were increased. There was no significant change in the levels of these three cytokines in the supernatant of macrophages after LPS stimulation. (2) The number of CFU E and CFU GM produced in the bone marrow cells increased significantly when more than 10% of the normal macrophages were added. The number of CFU E and CFU GM produced by the same proportion of radiation-injured macrophages decreased more significantly. (3) The number of CFU E and CFU GM produced by bone marrow cells excluding Mac 1+ cells increased, while the number of macrophages added again decreased. Conclusion The macrophages are activated after irradiation injury and the hematopoietic inhibitory activity is enhanced. This may be one of the reasons for the suppression of hematopoietic function of bone marrow in radiation injury.