Abstract
We investigated the protective properties of diphlorethohydroxycarmalol (DPHC), a phlorotannin, against ultraviolet B (UVB) radiation-induced cyclobutane pyrimidine dimers (CPDs) in HaCaT human keratinocytes. The nucleotide excision repair (NER) system is the pathway by which cells identify and repair bulky, helix-distorting DNA lesions such as ultraviolet (UV) radiation-induced CPDs and 6-4 photoproducts. CPDs levels were elevated in UVB-exposed cells; however, this increase was reduced by DPHC. Expression levels of xeroderma pigmentosum complementation group C (XPC) and excision repair cross-complementing 1 (ERCC1), which are essential components of the NER pathway, were induced in DPHC-treated cells. Expression of XPC and ERCC1 were reduced following UVB exposure, whereas DPHC treatment partially restored the levels of both proteins. DPHC also increased expression of transcription factor specificity protein 1 (SP1) and sirtuin 1, an up-regulator of XPC, in UVB-exposed cells. DPHC restored binding of the SP1 to the XPC promoter, which is reduced in UVB-exposed cells. These results indicate that DPHC can protect cells against UVB-induced DNA damage by inducing the NER system.
Highlights
Ultraviolet B (UVB) radiation (280–320 nm), a component of sunlight, can cause severe damage to skin cells and even induces skin cancer [1]
70%–80% of the total UV-induced photoproducts, we determined the effect of DPHC on UVB-induced cyclobutane pyrimidine dimers (CPDs) production by dot-blot analysis with a CPD antibody
These results indicate that DPHC protects HaCaT cells against UVB-induced CPDs
Summary
Ultraviolet B (UVB) radiation (280–320 nm), a component of sunlight, can cause severe damage to skin cells and even induces skin cancer [1]. UVB radiation is one of the most important causes of three major classes of DNA lesions: cyclobutane pyrimidine dimers (CPDs), pyrimidine 6-4 pyrimidone photoproducts (6-4PPs), and their Dewar isomers [2]. Various DNA repair pathways respond to DNA damage induced by oxidative stress and exposure to environmental factors such as UV radiation. The canonical nucleotide excision repair (NER) pathway removes helix-distorting nucleotide lesions, including UV light-induced CPDs. Mutations in genes of the NER pathway, including xeroderma pigmentosum group C (XPC) and excision repair cross complementation group 1 (ERCC1), are associated with elevated risk for various cancers.
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