Quercetin inhibits human microvascular endothelial cells viability, migration and tube-formation in vitro through restraining microRNA-216a

Abstract

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.

Keywords:

• Peripheral arterial disease
• quercetin
• microRNA-216a
• PI3K/AKT
• JAK2/STAT3

Disclosure statement

The authors declare that there are no conflicts of interest.