血管内皮功能紊乱是糖尿病血管病变的始动环节。内皮微颗粒（EMPs）是内皮损伤的标记物，可携带miRNAs介导细胞间信号传导，参与调控内皮细胞功能。然而，EMPs携带miRNAs参与糖尿病血管内皮损伤的机制尚未阐明。前期我们发表文章报道，胱硫醚-γ-裂解酶/硫化氢（CSE/H2S）系统具有广泛的心脏保护作用。我们通过基因芯片筛查发现糖尿病患者EMPs的miR-26较正常明显升高，生物信息学预测miR-26靶基因是CSE，而CSE/H2S系统受损加重高糖诱导的内皮细胞损伤。基于此，我们提出“EMPs携带的miR-26靶向调控内皮细胞的CSE/H2S系统，加重糖尿病血管内皮损伤”的假设，从动物、细胞、分子多层次观察高糖环境下EMPs携带miR-26对血管内皮功能的作用，探讨EMPs/miR-26调控CSE/H2S系统及下游MAPK/NF-κB通路机制，为糖尿病内皮功能障碍的治疗提供新干预靶点。

Dysfunction of vascular endothelial cells is the initiating factor of the development of diabetic vascular dysfunction. Endothelial microparticles (EMPs) are markers of endothelial injury, which can also serve as a carrier of miRNAs to regulate endothelial function. However, the exact mechanism of miRNAs-containing EMPs in diabetic vascular endothelial dysfunction has not yet been elucidated. We previously published articles reported that cystathionine -γ- lyase/ hydrogen sulfide (CSE/H2S) system has extensive cardiac protection effect. We have found that miR-26 expression in serum EMPs was significantly higher in diabetic patients compared with normal controls using miRNAs arrays，and bioinformatics predicted the target genes of miR-26 was CSE. Moreover, CSE/H2S system impairment could aggravate high glucose induced endothelial cell injury. Based on these, we assumed that "miR-26 in EMPs targeted CSE/H2S system in endothelial cells, which would aggravate the diabetic vascular endothelial injury", we would observe the relationship between miR-26 in EMPs and vascular endothelial function under high glucose environment in animals, cells, tissues and molecules levels, and to explore its regulatory mechanism involving CSE/H2S system and its related MAPK/NF-κB signaling pathway. Our research may provide new clues and intervention targets for the treatment of diabetic endothelial dysfunction.