基于CaSR介导的EPCs-VSMC信息传递探讨人参皂苷Rg1促血管损伤修复作用机制

内皮细胞损伤和平滑肌细胞（VSMC）表型转化所致血管重塑是血管损伤性疾病共同病理基础。内皮祖细胞（EPCs）通过自身分化和分泌功能的信息传递，直接参与血管内皮修复并抑制VSMC表型转化。钙敏感受体（CaSR）在EPCs表达并促进EPCs增殖、迁移和血管形成能力。前期研究发现Rg1抑制球囊损伤后血管内膜增生，机制与其动员骨髓EPCs，促进内皮修复，抑制VSMC增殖有关，并发现CaSR抑制剂降低Rg1的作用。但CaSR在Rg1促血管损伤修复中具体作用机制尚不明确。推测CaSR介导EPCs-VSMC信息传递，在Rg1促进EPCs抑制VSMC表型转化中起重要作用。项目拟采用离体EPCs与VSMC共培养观察Rg1干预的EPCs对VSMC表型和功能的影响，探讨CaSR在Rg1干预EPCs-VSMC信息传递中的作用，并采用动物血管内皮损伤模型进行验证，为内皮损伤性血管疾病探索有效防治手段和早期干预策略。

Vascular remodeling caused by vascular endothelial cell injury and phenotype transformation of vascular smooth muscle cell (VSMC) are the common pathophysiological basis of vascular injury disease. Endothelial progenitor cells (EPCs) are directly involved in vascular endothelial repair and inhibition of VSMC phenotype transformation through self-differentiation and information transmission of secretory function. Calcium sensing receptor (CaSR) is expressed in EPCs and promotes the proliferation, migration and angiogenesis of EPCs. Our previous study found that ginsenoside Rg1 inhibited vascular intimal hyperplasia after balloon injury, and the mechanism was related to the effect of Rg1 on the mobilization of bone marrow EPCs, promotion of endothelial repair and inhibition of VSMC proliferation. We also found that CaSR inhibitor reduced the effect of Rg1. However, the specific mechanism of CaSR in Rg1 promoting vascular repair is not clear. We speculate that CaSR mediates the information transfer of EPCs-VSMC and plays an important role in Rg1 promoting the inhibition of phenotype transformation of VSMC by EPCs. The purpose of this project is to examine the effect of Rg1 intervention on EPCs and the phenotype and function of VSMC by co-culture of EPCs and VSMC in vitro, to explore the role of CaSR in Rg1 intervention on the information transmission of EPCs-VSMC, and to verify the mechanism by animal vascular endothelial injury model, so as to explore effective prevention and treatment methods and early intervention strategies for vascular diseases with endothelial injury.