Apigenin prevents ultraviolet-B radiation induced cyclobutane pyrimidine dimers formation in human dermal fibroblasts.

Exposure to solar ultraviolet-B (UVB) radiation leads to the formation of cyclobutane pyrimidine dimers (CPDs). We investigated the protective effect of apigenin against UVB-induced CPDs formation in human dermal fibroblasts cells (HDFa). For this purpose, HDFa cells were treated with apigenin (15μM) prior to UVB irradiation (20mJ/cm2); DNA damage and subsequent molecular end points were observed. Exposure to UVB radiation increased significant CPDs formation in HDFa cells and the frequencies of CPDs were reduced by treatment with apigenin (15μM). UVB-induced CPDs downregulates the expression of nucleotide excision repair (NER) genes such as xeroderma pigmentosum complementation group C, B, G and F (XPC, XPB, XPG and XPF), transcription factor II human (TFIIH) and excision repair cross-complementation group 1 (ERCC1) in HDFa cells. Conversely, apigenin treatment restored UVB-induced loss of NER proteins in HDFa cells, which indicates its preventive effect against CPDs formation. Besides, single low dose UVB-exposure induced nuclear fragmentation, apoptotic frequency and apoptotic proteins expression (Bax and Caspase-3) have been prevented by the apigenin pretreatment. Furthermore, apigenin exhibits strong UV absorbance property and showed 10.08 SPF value. Thus, apigenin can protect skin cells against UVB-induced CPDs formation probably through its sunscreen effect. Hence, apigenin can be considered as an effective protective agent against UV induced skin damages.

Britto SM ，Shanthakumari D ，Agilan B ，Radhiga T ，Kanimozhi G ，Prasad NR ... -  《-》

Silibinin enhances the repair of ultraviolet B-induced DNA damage by activating p53-dependent nucleotide excision repair mechanism in human dermal fibroblasts.

Guillermo-Lagae R ，Deep G ，Ting H ，Agarwal C ，Agarwal R ... -  《Oncotarget》

Silymarin protects epidermal keratinocytes from ultraviolet radiation-induced apoptosis and DNA damage by nucleotide excision repair mechanism.

Katiyar SK ，Mantena SK ，Meeran SM 《-》

Protective Effect of Diphlorethohydroxycarmalol against Ultraviolet B Radiation-Induced DNA Damage by Inducing the Nucleotide Excision Repair System in HaCaT Human Keratinocytes.

Piao MJ ，Hewage SR ，Han X ，Kang KA ，Kang HK ，Lee NH ，Hyun JW ... -  《Marine Drugs》

Phloroglucinol enhances the repair of UVB radiation-induced DNA damage via promotion of the nucleotide excision repair system 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.

Piao MJ ，Ahn MJ ，Kang KA ，Kim KC ，Cha JW ，Lee NH ，Hyun JW ... -  《-》