黄芪注射液对骨髓抑制性贫血小鼠造血调控的实验研究

Study on Effect of Astragalus Membranaceus Injection on Hematopoiesis in Anemic Mice with Myelosuppression

目的观察黄芪注射液(Astragalus membranaceus injection,AMI)对放、化疗因素所致骨髓抑制性贫血小鼠造血的影响,并探讨其可能的机制。方法:采用Co^(60)照射、注射环磷酰胺、氯霉素复合造模建立贫血小鼠模型,并将动物随机分为三组:AMI给药组Ⅰ、Ⅱ和对照组,分别腹腔注射AMI[500 mg/kg、1000 mg/kg]或等量生理盐水,第7日全自动血球仪检测外周血和骨髓有核细胞,并应用免疫组化和造血祖细胞体外培养技术,检测骨髓有核细胞BcL-XL和BcL-2蛋白的表达及进行三系造血祖细胞集落计数。结果:AMI给药组Ⅰ的RBC、HB、PLT(P<0.05)和BM(P<0.01)明显高于贫血对照组;同时给药组Ⅰ的CFU-E、BFU-E、CFU-Meg和骨髓有核细胞抗凋亡蛋白BcL-XL 的表达也明显高于贫血对照组(P<0.05或P<0.01).给药组Ⅱ的CFU-E和骨髓有核细胞抗凋亡蛋白BcL-XL的表达也高于贫血对照组(P<0.05)。结论:黄芪注射液可以通过上调抗凋亡蛋白BcL-XL表达减轻骨髓有核细胞的凋亡,并促进红系、巨核造血。

Objective： To investigate the effect of AMI on hematopoiesis in anemic mice and explore the possible mechanisms. Methods： Anemic mice model resulted from myelosuppression by irradiation and cytotoxic chemotherapeutic compounds were randomly divided into three groups： treated group Ⅰ, treated group Ⅱ and anemic control group. Intraperitoneal doses of AMI （500 mg/kg, 1000 mg/kg） were given to the treated group, and equal doses of physiological saline were given to the anemic control group. On 7 days after treatment, the count of whole blood cells and bone marrow cells were determined by blood auto-analyzer. The numbers of CFU-GM （ granulocyte and macrophage colony forming unit）, CFU-E （ colony forming unit-erythroid）, BFU-E （ burst forming unit-erythroid）, CFU-Meg（colony forming unit-megakaryocyte） were determined by using technique of hematopoietic progenitor cells culture in vitro. Expression of anti-apoptosis protein BcL-XL and BcL-2 in BMC were determined by immunohistochemistry, Results： RBC,HB,PLT（P 〈 0. 05 ） and BMC （ P 〈 0. 01 ）in treated group I were significantly higher than that of anemic control. The number of CFU-E,BFU-E and CFU-Meg as well as expression of anti-apoptosis protein BcL-XL of BMC in treated group Ⅰ also were significantly higher than that of anemic control（P 〈0. 05 or P 〈0. 01 ）, while numbers of CFU-E as well as expression of anti-apoptosis protenin BcL-XL of BMC in treated group Ⅱ were higher than that of anemic control（ P 〈0. 05）. Conclusion： AMI can lesson apoptosis of bone marrow cells and promote hematopoietic progenitor cells to differentiate along the erythroid and megakaryocytoid line by up-regulating expression of antiapoptosis protein BcL-XL of BMC.