BACKGROUNDHemorrhoids refer to a common anorectal disorder that is usually associated with vascular proliferation. The present study investigated the role of miR-143-3p in the development of hemorrhoids and postoperative wound healing, aiming to provide novel ideas for the study of the pathogenesis of hemorrhoids and their clinical treatment.METHODSHemorrhoid tissues and normal perianal tissues were collected from 42 patients who underwent hemorrhoid surgery. The expressions of miR-143-3p, vascular endothelial markers (CD31, vWF, and VEGFR2), and inflammatory factors (TNF-α, IL-1β, and IL-6) in these tissues were determined using RT-qPCR. The correlation of miR-143-3p with CD31, vWF, and VEGFR2 was analyzed using Pearson's method. The proliferation of HUVEC and HaCaT cells was detected using the CCK-8 assay. The migration of HUVEC and HaCaT cells was detected using Transwell assay. The apoptosis of HUVEC cells was detected using flow cytometry.RESULTSReduced expression of miR-143-3p in hemorrhoid tissues was negatively correlated to the mRNA levels of CD31, vWF, and VEGFR2. The mRNA levels of CD31, vWF, and VEGFR2 in the HUVEC cells were reduced after miR-143-3p overexpression. Overexpression of miR-143-3p inhibited the proliferation and migration of HUVEC cells while promoting apoptosis in these cells. Upregulation of miR-143-3p decreased the mRNA levels of TNF-α, IL-1β, and IL-6 in HaCaT cells while promoting cell proliferation and migration in these cells.CONCLUSIONSDownregulation of miR-143-3p was noted in hemorrhoids, which could be linked to the regulation of angiogenesis. MiR-143-3p might have an anti-inflammatory role in postoperative wound healing.