补肾解毒活血法与益气补血法对骨髓抑制小鼠造血功能影响的比较研究

目的:比较补肾解毒活血法与益气补血法对环磷酰胺(CTX)所致骨髓抑制小鼠造血功能的影响及其作用机制的不同特点.方法:昆明种小鼠80只,随机分为4组,正常对照组、模型组、补肾解毒活血组(20.55 g·kg -1·d-1)和益气补血组(17.47 g·kg-1·d-1).采用CTX 100 mg·kg-1 ip,连续3d,制成骨髓抑制小鼠模型.各组于造模完成后次日开始ig连续10d.分别于造模前及造模后1,3,5,7,10,14 d动态检测外周血象；于末次给药次日后进行骨髓有核细胞计数(BMNC)及粒-单核系集落形成单位( CFU-GM)、红系集落形成单位(CFU-E)、和红系爆式集落形成单位(BFU-E)集落计数.结果:补肾解毒活血方和益气补血方均可明显升高模型小鼠的WBC,PLT,BMNC,可促进造血祖细胞(HPC)增殖,CFU-GM,CFU-E,BFU-E集落数均显著高于模型组(P＜0.01)；补肾解毒活血方对血小板的恢复优于益气补血方.结论:补肾解毒活血方和益气补血方均可促进骨髓造血祖细胞集落生成,具有减轻和改善化疗后骨髓抑制的效果,而前者尤可减轻血小板减少、促进其恢复；其作用机制可能在骨髓细胞分化过程或造血微环境等途径上有不同.

A Comparative Study of Bushen Jiedu Huoxue Recipe and Yiqi Buxue Recipe on the Impact of Hematopoiesis in Marrow-Depressed Mice

Objective: To observe the hematopoietic effects and mechanisms of Bushen Jiedu Huoxue recipe and Yiqi Buxue recipe in the marrow-depressed mice. Method: Eighty Kunming mice were randomly divided into 4 groups: normal control group, model group, Bushen Jiedu Huoxue group(20.55 g ·kg^-1 ·d^-1),Yiqi Buxue group (17.47 g ·kg^-1 ·d^-1). The marrow-depressed model was established by ip cyclophos-phamide (CTX)100 mg ·kg^-1 for 3 days. After model establishment, the mice were ig treated with different recipes for 10 days. Peripheral blood cells were counted by microcellcounter; bone marrow nucleated cell and the amount of colony forming unit-granulocyte-macrophage(CFU-GM),colony forming unit-erythrocyte(CFU-E)and brust forming unit-erythocyte (BFU-E) were counted to study the effects of the proliferation of hematopoietic progenitor cell (HPC)11 days after the successful model set. Result: The Bushen Jiedu Huoxue recipe and Yiqi Buxue recipe could increase the number of WBC,PLT,bone mallow nucleated cell(BMNC),promote the proliferation of hematopoietic progenitor cell(HPC).The quantities of CFU-GM,CFU-E,BFU-E were significantly higher than the model group(P<0.01). Conclusion: Both of Bushen Jiedu Huoxue and Yiqi Buxue can promote the colony formation of bone marrow hematopoietic progenitor cells, and alleviate the effect of bone marrow suppression after chemotherapy, while the former one was more significant in improving thrombocytopenia, to promote their recovery. Its mechanism may be vary in the bone marrow hematopoietic cell differentiation process or in the micro-environment.