Phloroglucinol enhances the repair of UVB radiation-induced DNA damage via promotion of the nucleotide excision repair system in vitro and in vivo

• UVB radiation leads to the DNA lesion, cyclobutane pyrimidine dimers (CPDs).
• Nucleotide excision repair (NER) is critical for the repair of CPDs.
• Phloroglucinol enhances the NER repair of UVB radiation-induced CPDs.
• NER repair by phloroglucinol occurs via action of XPC and ERCC1 in vitro and in vivo.

Exposure to solar UVB radiation can lead to the formation of DNA lesions such as cyclobutane pyrimidine dimers (CPDs). Nucleotide excision repair (NER) is critical for the repair of CPDs induced by UV radiation. The purpose of this study was to investigate the ability of phloroglucinol to protect against the formation of UVB-induced CPDs in vitro and in vivo. Exposure to UVB radiation increased the number of CPDs in both HaCaT keratinocytes and mouse skin; however, these increases were reduced by treatment with phloroglucinol. Expression levels of xeroderma pigmentosum complementation group C (XPC) and excision repair cross-complementation 1 (ERCC1), which are essential components of the NER pathway, were reduced following UVB exposure, although phloroglucinol treatment recovered these levels in both HaCaT keratinocytes and mouse skin. Phloroglucinol also inhibited UVB-induced reductions in binding of the transcription factors specificity protein 1 to the XPC promoter. These results demonstrate that phloroglucinol can protect cells against UVB-induced DNA damage by inducing NER.