血管新生是糖尿病皮肤溃疡愈合的关键。目前研究发现黄芪甲苷能促进血管新生，但作用机制不详。课题组前期研究发现黄芪甲苷促内皮祖细胞分泌的外泌体（EPC-Exos）可被内皮细胞摄取以增强其成管功能；进一步在预实验中研究发现所分泌的EPC-Exos富含miR-126，且经靶基因预测发现PIK3R2和SPRED1为miR-126调控血管新生潜在靶基因。综合前期研究结果，课题组推测黄芪甲苷介导的EPC-Exos负载miR-126调控PIK3R2/SPRED1发挥血管新生作用。本研究将以“EPC-Exos→miR-126-PIK3R2/SPRED1信号轴→血管新生”为主线，从分子生物学、细胞生物学及实验动物水平探讨黄芪甲苷介导的EPC-Exos对高糖受损内皮细胞和糖尿病皮肤溃疡血管新生相关蛋白基因表达、内皮细胞增殖和创面血管化的影响，以阐明其作用的具体信号通路及机制，为黄芪甲苷用于创面修复提供理论依据。

Angiogenesis is the key of diabetic skin ulcers heal. The current research finds that astragaloside IV can promote angiogenesis, but the mechanism is unknown. Research group early found that exosomes secreted by endothelial progenitor cells(EPC-Exos)induced by astragaloside IV could be absorbed by endothelial cells to enhance its tubulogenic function; further in the preliminary experiment, it was found that the secreted EPC-Exos were rich in miR-126, and PIK3R2 and SPRED1 were found to be potential target genes regulating angiogenesis of miR-126 through target gene prediction. In the comprehensive preliminary study, the research group speculated that astragalosis-mediated EPC-Exos loaded miR-126 and regulates the PIK3R2/SPRED1 signaling axis to play a role in angiogenesis. This study will use "EPC-Exos miR-126-PIK3R2/SPRED1 signal axis angiogenesis" as the axis, disscuss the effect on EPC-Exos mediated by astragaloside IV to the expression of angiogenic proteins and genes in hyperglycemia damaged endothelial cells and diabetic skin ulcers, endothelial cell proliferation and destroyed surface vascularization from molecular biology, cell biology and experimental animal level, to elucidate the specific signal pathway and mechanism of its action, and provide theoretical basis for astragaloside IV used for destroyed surface repair.