摘要Objective:To investigate the effects of panax notoginseng saponins (PNS) on homing of C-kit+ bone mesenchymal stem cells (BMSCs) to the infarction heart.Methods:The acute myocardial infraction (AMI) model was established in 140 Wistar rats,105 model rats survived after operation,and the model rats were randomly divided into five groups,21 rats in each group:Western medicine group mobilized by subcutaneous injection of human granuloctye colony stimulating factor (G-CSF) 50 μg·kg-1·d-1;sham operation group and a model group treated by subcutaneous injection of normal saline 50 μg·kg-1·d-1; Chinese medicine group mobilized by intraperitoneal injection of Xuesaitong (血 塞通) (ingredients of PNS) 150 mg·kg-1·d-1;integrative medicine group mobilized by subcutaneous injection of G-CSF 50 μg·kg-1·d-1 and intraperitoneal injection of Xuesaitong 150 mg·kg-1·d-1.Except for the sham-operated group,each group was divided into three sub-groups by three time points of 1 d,7 d and 14 d.G-CSF was injected once a day for 7 d.Xuesaitong was injected once a day until the rats were killed.The flow cytometry was used for detection of C-kit + cells in the peripheral blood in different time points,and immunohistochemical method was used for detection of the changes of C-kit + cell and Ki-67+ cell numbers in the marginal zone of AMI.Results:Twenty-four hours after the operation,C-kit + cells had a slight increase in the model group compared with the sham operation group (P＞0.05).The peripheral blood C-kit+ cells in the integrative group increased significantly compared with the other groups on 7 d and 14 d (all P＜0.05).Meanwhile the expression of C-kit+ cells and Ki-67+ cells in the marginal zone of AMI in the integrative group increased significantly compared with the Chinese medicine group,the western medicine group and the model group on 1 d,7 d and 14 d (all P＜0.05),and the cells in the integrative group decreased significantly on 14 d compared with that on 7 d (P＜0.05).Conclusion:PNS can cooperate with G-CSF to mobilize C-kit+ BMSCs from the marrow into the peripheral blood and promote them "homing" to the infarction heart.