Fermented black ginseng extract prevents UVB‐induced inflammation by regulating the nc886‐PKR pathway in human keratinocytes

Background Continuous exposure of the skin to ultraviolet B (UVB) rays can cause inflammation and photodamage. In previous studies, we observed that the upregulation of nc886, a noncoding RNA (ncRNA), can alleviate UVB‐induced inflammation through suppression of the protein kinase RNA (PKR) pathway. We aim to investigate the effect of fermented black ginseng extract (FBGE), which has been shown to increase the expression of nc886, on UVB‐induced inflammation in keratinocytes. Methods To confirm the cytotoxicity of FBGE, MTT assay was performed, and no significant cytotoxicity was found on human keratinocytes. The efficacies of FBGE were assessed through qPCR, Western blotting, and ELISA analysis which confirmed regulation of UVB‐induced inflammation. Results The analysis results showed that FBGE inhibited the decrease in nc886 expression and the increase in the methylated nc886 caused by UVB. It also prevented the UVB‐induced increase of metalloproteinase‐9 (MMP‐9), metalloproteinase‐1 (MMP‐1), cyclooxygenase‐2 (COX‐2), prostaglandin E2 (PGE2), interleukin‐8 (IL‐8) and tumor necrosis factor‐α (TNF‐α). Additionally, FBGE suppressed the PKR‐MAPK pathways activated by UVB. Conclusion These results implicate that FBGE can alleviate UVB‐induced inflammation through regulation of the nc886‐PKR pathway.