文献类型：期刊文献

中文题名：补虚化瘀方对联合化疗荷瘤小鼠骨髓造血功能的影响

英文题名：Effect of Buxu Huayu Prescription on Myeloid Hematopoiesis in Tumor -bea ring Mice After Combined Chemotherapy

作者：田卫卫[1];李偶[2];黄映红[3];邓道昌[3];王庆苗[4]

第一作者：田卫卫

机构：[1]解放军第452医院血液科,成都610021;[2]四川华神药业股份有限公司,成都610075;[3]成都中医药大学,成都610075;[4]甘肃中医学院,兰州730000

第一机构：解放军第452医院血液科,成都610021

年份：2003

卷号：14

期号：1

起止页码：3

中文期刊名：中药新药与临床药理

外文期刊名：Traditional Chinese Drug Research and Clinical Pharmacology

收录：CSTPCD;;CSCD:【CSCD_E2011_2012】；

基金：四川省中医管理局资助项目(编号96-266)。

语种：中文

中文关键词：补虚化瘀方;药理学;阿糖胞苷;副作用;环磷酰胺;骨髓抑制;中药疗法;疾病模型

外文关键词：Buxu Huayu Prescription /pharmacology;Cytarabine /adverse effects;Cyclo phosphamide /adverse ef-fects;Arrest of bone marrow /TCD therapy;Disease models,animal

摘要：目的观察补虚化瘀方对联合化疗荷瘤小鼠骨髓造血的作用。方法采用P388瘤株造成荷瘤小鼠模型后,再以环磷酰胺、阿糖胞苷腹腔注射获得联合化疗荷瘤小鼠骨髓抑制模型,实验分为正常组、模型组及补虚化瘀方组,进行血常规、骨髓有核细胞(BMC)计数、粒单系祖细胞(CFU-GM)集落计数、骨髓细胞增殖能力测定。结果联合化疗可致荷瘤小鼠血红蛋白(Hb)、白细胞计数(WBC),BMC、CFU-GM集落计数及骨髓细胞增殖能力明显低于正常组(P<0.01),补虚化瘀方可提高联合化疗荷瘤小鼠外周血Hb、WBC数,提高BMC、CFU-GM集落计数及骨髓细胞增殖能力(P<0.01)。结论补虚化瘀方对联合化疗荷瘤小鼠骨髓抑制模型具有保护造血细胞和促进其化疗损害后的修复作用。
Objective To observe the effects of Buxu Huayu P rescription(BHP)on myeloid hematopoiesis in tumor -b ear-ing mice after combined chemotherap y.Methods Tumor -bearing mouse models were established by implanting P388tu-mor strain and the arrest of myeloid h ematopoiesis in the models was induced by intraperitoneal injection of c yclophos-phamide(CTX)and cytarabine(Ara -c ).The mice were allocated to 3groups:the normal control group,the model group and BHP group.Peripheral bloo d cell count,bone marrow karyocytes(BMK)count,colony count of progenitors o f granulocytes /monocytes(CCP -GM)and the proliferation of bone marrow cells(BMC)were examined.Results The combination of CTX and Ara -c could decrease plasma hemoglobin(Hb )content,the number of white blood cells(WBC),BMK and CCP -GM and the proliferatio n of BMC in model mice(P<0.01as compared with normal control group).And BHP could counteract the above e ffect induced by the combined chemotherapy(P<0.01).Conclusion BHP has an effect in protecting myelo id hematopoietic cells from chemoth erapeutic damage and promoting the r ehabilita-tion of bone marrow after chemothera py.