骨髓间充质干细胞（MSCs）移植治疗糖尿病性勃起功能障碍（DMED）有致瘤性、疗效短等缺点，因而无细胞治疗是目前研究热点。近期多聚焦于外泌体（exosome）应用。我们前期发现：增强的氧化应激状态及导致的血管内皮细胞和平滑肌细胞功能不全是DMED主要原因；激活Nrf2基因能改善糖尿病大鼠勃起功能。最新研究发现MSCs-exosomes介导miR-210能改善受体局部氧化应激水平，推测与激活PI3K/AKT有关。国内外尚未有miR-210治疗DMED的报道。因此，我们提出局部注射MSCs-exosomes介导miR-210治疗DMED的假设。本项目拟以PI3K/AKT/Nrf2通路改变为切入点，按照分子-细胞-整体水平，体内、外实验结合的方法，探究miR-210对糖尿病性阴茎海绵体氧化应激状态的作用，以及阴茎海绵体血管内皮细胞功能、平滑肌细胞功能变化情况，探索DMED无细胞治疗的新思路。

The transplantation of bone marrow mesenchymal stem cells (MSCs) in the treatment of diabetic erectile dysfunction (DMED) has the shortcoming of tumorigenicity and short curative effect. Therefore, acellular therapy is the research direction at present. Recent focus on this issue is the application of exosomes. Our previous studies have found that the dysfunction of vascular endothelial cells and smooth muscle cells caused by the increased oxidative stress may be the main pathogenesis of DMED. We also found activation of Nrf2 gene could significantly improve erectile function of diabetic rats. Recent studies have found that miR-210 mediated by MSCs-exosomes can improve the local oxidative stress microenvironment, which is presumably related to activation of PI3K/AKT pathway. Up to now, there are no reports on the mechanism of miR-210 treatment for DMED. Therefore, we propose that local injection of miR-210 mediated by MSCs-exosomes is more effective in the treatment of DMED. The study intends to study the change of PI3K/AKT/Nrf2 pathway. In vivo and in vitro experiments will be combined according to the molecular-cell-organism level. We will explore the effect of miR-210 on the oxidative stress state of cavernous body and the changes of vascular endothelial cell function and smooth muscle cell function in the cavernosum. The study is aimed to explore a new acellular therapy for DMED.