The aim of this study was to investigate the mechanisms by which troxerutin protects cells against ultraviolet B (UVB) radiation. First, we demonstrate that pre-treatment with troxerutin protects normal human dermal fibroblasts (nHDFs) against UVB-induced cytotoxicity. As shown by migration assay and DNA repair analysis, troxerutin increased cell migration and DNA repair activity in the nHDFs. Subsequently, we analyzed microRNA (miRNA) expression profiles in the nHDFs. miRNAs are 19- to 24-nucleotide (nt) non-coding RNA molecules that regulate the translation of target genes through RNA interference. In UVB-exposed cells, miRNAs act on crucial functions, such as apoptosis and cellular senescence. miRNA expression is significantly altered during the protective process induced by phytochemicals. Therefore, understanding changes that occur in miRNA expression profiles may help to elucidate the protective mechanisms of troxerutin. We identified 11 miRNAs that were significantly (>2-fold) upregulated and 12 that were significantly downregulated (>2-fold) following treatment of the nHDFs with troxerutin. In addition, we investigated the biological functions of these miRNAs through the prediction of miRNA targets and Gene Ontology analysis of the putative targets. Overall, our findings indicate that pre-treatment with troxerutin increases the viability of UVB-exposed nHDFs through the alteration of the miRNA expression profiles.

Ultraviolet (UV) radiation induces severe alterations in the molecular and cellular components of normal human dermal fibroblast (NHDF) cells by disrupting many intracellular transduction cascades. Although UV responses have been well documented at the genome and proteome levels, UV protective effects have not been elucidated at these levels. The aim of the present study was to demonstrate that arctiin, a phytochemical isolated from the plant Arctium lappa, induced a protective effect against UVB radiation by changing microRNA (miRNA) expression profiles. Using flow cytometry, and water-soluble tetrazolium salt (WST-1)-based cell viability, wound healing, and DNA repair assays we showed that pretreatment with arctiin prior to UVB irradiation reduced UVB-induced apoptosis, cell migration defects, and DNA damage in NHDF cells. It was also found that arctiin‑induced UVB protection is associated with altered miRNA expression profiles. Bioinformatic analysis revealed that the deregulated miRNAs were functionally involved in mitogen-activated protein kinase (MAPK) signaling and cancer signaling pathways. The results suggest that arctiin acts as a UVB protective agent by altering specific miRNA expression in NHDF cells.