鲜红斑痣是一种先天性、进行性皮肤毛细血管畸形，严重影响患者美观和社会交往，临床疗效欠佳。我们临床发现伊曲康唑对鲜红斑痣潜在有效。通过原代HUVECs，我们研究发现伊曲康唑抑制血管形成；mRNA基因芯片分析筛选出伊曲康唑显著上调白介素IL-24；rhIL-24抑制血管形成，验证IL-24具有重要功能。伊曲康唑为AMPK新型激活剂。前期，我们研究发现伊曲康唑、rhIL-24处理原代HUVECs后ROS升高；伊曲康唑、H2O2处理后上调p-AMPK；伊曲康唑上调IL-24，抑制p-mTOR和VEGF。以上结果提示：伊曲康唑上调IL-24产生ROS激活AMPK，抑制下游mTOR/VEGF，抑制鲜红斑痣血管生成。综上，通过细胞、动物模型结合临床病理组织，综合多种分子生物学技术，探究伊曲康唑调控IL-24抑制鲜红斑痣血管生成的生物学功能和作用机制，阐明IL-24作为鲜红斑痣临床治疗靶点的潜在价值。

Port wine stain is a congenital and progressive skin capillary malformation with poor clinical effect, which seriously affects the patients' appearance and social interaction. We found that itraconazole is potentially effective in the treatment of port wine stains. Taking the endothelial cells of umbilical vein (primary HUVECs) as the cell model of port wine stains, we found that itraconazole inhibited angiogenesis; mRNA microarray analysis showed that itraconazole significantly upregulated IL-24; exogenous recombinant human IL-24 (rhIL-24) inhibited angiogenesis, which verified that IL-24 had important functions. Itraconazole is a new activator of AMPK. In the early stage, the ROS level of HUVECs treated with itraconazole or rhIL-24 was increased; the AMPK phosphorylation level of primary HUVECs treated with itraconazole or H2O2 was up-regulated; the expression of IL-24 were up-regulated by itraconazole, however, the expression of p-mTOR and VEGF was inhibited. These results suggested that itraconazole up regulated the production of ROS by IL-24 to activate AMPK, thus inhibiting the downstream mTOR/VEGF to reduce the angiogenesis of port wine stains. On the basis of all above, through cell model, animal model and clinical pathological tissue, combined with multiple molecular biological technologies, the biological functions and mechanisms of itraconazole regulating IL-24 to inhibit the angiogenesis of port wine stains were studyed deeply, and the potential value of IL-24 as the clinical treatment target of port wine was clarified.