何首乌提取物对放射线照射小鼠血小板生成的保护作用

Protective Effect of Shouwu on Thrombocytopoiesis in Irratiated Mice

目的:探讨何首乌提取物对放射线照射后小鼠血小板(Plt)生成功能的促进作用。方法:24只BALB/C小鼠随机分为正常组(A组。不接受照射和药物处理),对照组(B组)和何首乌提取物组(C组),每组8只。B、C组予3.5Gy Cs137射线全身照射;照射后C组每天腹腔注射何首乌提取物125mg.kg-1.d-1,连续21 d,B组注射等容积NS。于照射前及照射后第7、14、21 d采集尾部静脉血,观察全血细胞计数变化;第21 d采血后取骨髓行巨核细胞集落形成(CFU-MK)、骨髓基质细胞集落形成(CFU-F)、红系爆增性集落形成(BFU-E)及粒单系集落形成(CFU-GM)培养。观察6只正常小鼠体外骨髓CFU-MK、CFU-F在不同浓度(0、10、50、100、200、500μg/mL)何首乌提取物作用下的生长情况。结果:C组Plt计数回升明显高于B组(P<0.01),体内C组的CFU-MK、CFU-F、BFU-E、CFU-GM集落生长明显优于B组(P<0.05,P<0.01)。体外小鼠骨髓CFU-F的生长对何首乌提取物有浓度-依赖性。而何首乌提取物对体外骨髓CFU-MK生长无明显作用。结论:何首乌提取物对照射后小鼠骨髓的Plt生成功能有促进作用,它的作用机制可能通过刺激骨髓基质细胞增殖,改善巨核细胞造血微环境,进而提升外周血Plt数量。

Objective：To study the protective effect of Shouwu on thrombocytopoiesis in irradiated mice.Methods：Altogether 24 BALB/C mice were randomly divided into Group A（received neither irradiation nor Shouwu）,3.5 Gy gama-ray was received between Group B and C.After irradiation,according to dosage of 125 mg·kg-1·d-1,Shouwu was injected intraperitoneally to Group C until 21 days,and Group B received same volume saline.The peripheral blood platelet,white blood cell（WBC）,and red blood cell（RBC）were counted from three groups at day0,day 7,day 14,and day 21.All the mice were sacrificed on day 21,the bone marrow cell was collected for culture of colony forming unit-megakaryocyte（CFU-MK）,colony forming unit-fibroblast（CFU-F）,colony forming unit-erythroid（BFU-E）,colony forming unit-granulocytemacrophage（CFU-GM）.The effect of Shouwu on CFU-MK and CFU-F formation at different doses（0,10,50,100,200,500 μg/mL）in vitro was investigated.Results：The platelet count in Group C was significantly higher than Group B（P0.01）.In vivo,CFU-MK,CFU-F,BFU-E and CFU-GM in Group C were dramatically better than those of Group B（P0.05,P0.01）.Shouwu directly exerted proliferative effect on in vitro stromal cell of bone marrow as a dose-dependent manner excluding megakaryocyte linage.Conclusion：Shouwu has protective effect on thrombo-cytopoiesis in irradiated mice.The protective mechanism may be mediated via improvement of local hematopoietic microenvironment or upregulation of 5-HT product.