[关键词]
[摘要]
目的 考察红景天苷对环磷酰胺(Cyclophosphamide,CTX)致骨髓损伤小鼠骨髓造血和外周血象的影响。方法 84只昆明小鼠随机分为6组,即正常对照组,模型组,茜草双酯组(100 mg·kg-1),红景天苷低、中、高剂量组(20,40,80 mg·kg-1)。用CTX按50 mg·kg-1剂量对小鼠腹腔注射,每天1次,连续5 d,复制骨髓损伤模型小鼠,模型复制后第1次给予CTX后,立即口服灌胃给予红景天苷,每天1次,连续10 d,在0,1,3,5,7,9,11,14 d检测外周血象,在第10天进行骨髓细胞集落培养和血清造血因子测定。结果 与模型组比较,红景天苷对CTX致骨髓损伤小鼠骨髓中红系祖细胞(CFU-E、BFU-E)、粒系祖细胞(CFU-GM)数量的回升有明显促进作用(P < 0.05);可以提高血清中粒细胞集落刺激因子(G-CSF)、促红细胞生成素(Epo)的水平(P < 0.05);对CTX致骨髓损伤小鼠外周血白细胞和血小板的恢复有明显的促进作用(P < 0.05)。结论 红景天苷可提高造血因子水平,促进骨髓造血,进而升高外周血中的白细胞和血小板,提示红景天苷对CTX致骨髓损伤小鼠具有保护作用。
[Key word]
[Abstract]
Objective To investigate the effect of salidroside on marrow hematopoiesis and peripheral blood hemotology in mice with marrow injury induced by cyclophosphamide(CTX). Methods Eighty-four Kunming mice were randomly divided into 6 groups,normal group,model group,rubidate(100 mg·kg-1) group,and low-,middle-,and high- salidroside groups(in the dosage of 20,40,80 mg·kg-1,respectively). Mice model of marrow injury was established by intraperitoneal injection with CTX 50 mg·kg-1 once a day for five continuous days. After first medication of CTX,the mice were given gastric infusion of salidroside once a day for 10 continuous days. On day 0,1,3,7,9,11,and 14,the peripheral blood hematology was investigated. On day 10,hematopoietic progenitor colony-forming cells were assayed and serum hematopoietic factors were detected. Results Salidroside could increase the number of erythroid burst forming unit(BFU-E),erythroid colony forming unit(CFU-E),neutrophils and colony-forming unit- granulocyte macrophage(CFU-GM),and elevate granulocyte colony-stimulating factor(G-CSF) and erythropoietin(Epo) levels in CTX-induced marrow injury mice(P < 0.05). Salidroside could also increase the number of white blood cells(WBC) and blood platelets(PLT) in marrow injury mice(P < 0.05). Conclusion Salidroside has protective effect on CTX-induced marrow injury mice,and the mechanism may be related with the recovery of marrow hematopoiesis through increasing hemopoiesis factors.
[中图分类号]
R285.5
[基金项目]
湖州市科技计划项目(2011YS09)。