Background: Quercetin belongs to the flavonoids family, which has been proven to have extensive pharmacological effects. Nevertheless, the function of quercetin in peripheral arterial disease (PAD) has not yet been reported. In the research, we purposed to disclose the effectiveness of quercetin in the pathogenesis of PAD.

Methods: HMEC-1 cells were cultivated in Matrigel for 24 h to observe the tube-formation. Detections of cell viability, migration and apoptosis were through implementing CCK-8, Transwell and flow cytometry methods. Western blot was utilised for measuring angiogenesis-, migration- and apoptosis-correlative factors. MiR-216a expression was examined via qRT-PCR, and its functions in HMEC-1 cells were uncovered after miR-216a mimic transfection. Assessment of JAK2/STAT3 and PI3K/AKT pathways was via implementing western blot.

Results: HMEC-1 cells were spontaneously vascularised under Matrigel condition. Quercetin predominantly repressed cell viability, migration, VEGF expression and facilitated apoptosis in HMEC-1 cells. Additionally, suppression of miR-216a was discovered in HMEC-1 cells after quercetin stimulation, meanwhile miR-216a overexpression annulled the functions of quercetin in HMEC-1 cells. Besides, quercetin deactivated PI3K/AKT and JAK/STAT pathways through adjusting miR-216a.

Conclusion: The above-mentioned consequences exhibited that quercetin suppressed HMEC-1 cell viability, migration and tube-formation through hindering JAK2/STAT3 and PI3K/AKT pathway via declination of miR-216a.

背景：槲皮素属于类黄酮家族，已被证明具有广泛的药理作用。然而，槲皮素在外周动脉疾病（PAD）中的作用尚未见报道。本研究旨在揭示槲皮素在PAD发病机制中的作用。

方法：将HMEC-1细胞在Matrigel中培养24 h，观察试管形成情况。通过实施CCK-8、Transwell和流式细胞术方法检测细胞活力、迁移和凋亡。蛋白质印迹用于测量血管生成、迁移和细胞凋亡相关因子。通过qRT-PCR 检测MiR-216a 的表达，并在 miR-216a 模拟物转染后发现其在 HMEC-1 细胞中的功能。JAK2/STAT3 和 PI3K/AKT 通路的评估是通过实施蛋白质印迹。

结果： HMEC-1 细胞在基质胶条件下自发形成血管。槲皮素主要抑制 HMEC-1 细胞的细胞活力、迁移、VEGF 表达并促进细胞凋亡。此外，在槲皮素刺激后在 HMEC-1 细胞中发现了 miR-216a 的抑制，同时 miR-216a 过表达使 HMEC-1 细胞中槲皮素的功能无效。此外，槲皮素通过调节 miR-216a 使 PI3K/AKT 和 JAK/STAT 通路失活。

结论：上述结果显示出，槲皮素抑制HMEC-1细胞存活率，迁移和管形成通过阻碍JAK2 / STAT3和PI3K / AKT途径经由的miR-216a的偏角。