人参皂苷Rg1动员骨髓干细胞预防血管再狭窄的作用及机制研究

球囊损伤血管内膜的再内皮化是预防经皮冠状动脉血管腔内成形术（PTCA）术后血管平滑肌细胞（VSMC）移行和异常增殖所致血管再狭窄的关键环节；骨髓干细胞动员，并定向血管损伤部位迁移、分化可加速受损血管内膜的修复。项目组前期研究发现，人参皂苷Rg1可促进骨髓干细胞的增殖和向外周的动员，并且对球囊损伤后血管内膜异常增生具有明显的抑制作用。而Rg1是否通过动员骨髓干细胞归巢定位到血管损伤部位参与内皮修复及其调控机制是尚未阐明的关键问题。本项目拟采用大鼠颈动脉球囊损伤模型模拟临床PTCA术后血管内膜损伤，确证人参皂苷Rg1促进球囊损伤后血管内膜再内皮化修复，预防血管再狭窄作用；以血管损伤部位微环境和钙敏感受体（CaSR）信号通路为靶点探讨Rg1干预骨髓干细胞动员、归巢和分化参与球囊损伤后血管内皮修复及其调控机制，为Rg1用于临床防治血管再狭窄提供药理学依据。

The intima renovation is a key of vascular restenosis when vascular smooth muscle cells (VSMC) migration and proliferation after percutaneous coronary arterial lumen angioplasty (PTCA). Bone marrow stem cells mobilization、migration and differentiation can accelerate the damaged vascular intimal renovation. The research team found that, ginsenoside Rg1 can inhibits the neointimal hyperplasia when balloon injury via promoting the proliferation, mobilization and homing of bone marrow stem cells. However, the mechanism of Rg1 promoting the proliferation, mobilization and homing to participate in vascular injury endothelial repairing is unknown. This project intends to use rat carotid artery balloon injury models to corroborate the effect of Rg1 on the intima renovation and the prevention of vascular restenosis. And explore the mechanism of Rg1 intervention bone marrow stem cells mobilization, homing and differentiation in balloon injury endothelial and the regulatory mechanism of micro environment and CaSR signal pathway.