Abstract

Ulva lactuca (U. lactuca) is a green alga distributed worldwide and used as a food and cosmetic material. In our previous study, we determined the effects of U. lactuca methanol extracts on the UVB-induced DNA repair. In the present study, we fractionated U. lactuca methanol extracts to identify the effective compound for the DNA repair. MTT assay demonstrated that (+)-epiloliolide showed no cytotoxicity up to 100 μM in BJ-5ta human dermal fibroblast. Upon no treatment, exposure to UVB 400 J/m2 decreased cell viability by 45%, whereas (+)-epiloliolide treatment for 24 h after UVB exposure significantly increased the cell viability. In GO and GESA analysis, a number of differentially expressed genes were uniquely expressed in (+)-epiloliolide treated cells, which were enriched in the p53 signaling pathway and excision repair. Immunofluorescence demonstrated that (+)-epiloliolide increased the nuclear localization of p53. Comet assay demonstrated that (+)-epiloliolide decreased tail moment increased by UVB. Western blot analysis demonstrated that (+)-epiloliolide decreased the levels of p-p53, p21, Bax, and Bim, but increased that of Bcl-2. Reverse transcription PCR (RT-PCR) demonstrated that (+)-epiloliolide decreased the levels of MMP 1, 9, and 13, but increased that of COL1A1. These results suggest that (+)-epiloliolide regulates p53 activity and has protective effects against UVB.

Highlights

  • Sunlight includes visible rays, infrared rays, and ultraviolet light (UV)

  • DNA excision repair genes related to nucleotide excision repair (NER) involve in growth arrest and DNA damage α (Gadd45α), p48-XPE, and DNA polymerase, which are regulated by p53 [17]

  • (+)-Epiloliolide isolation was performed in three steps using U. lactuca methanol extracts (Figure 1)

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Summary

Introduction

Sunlight includes visible rays, infrared rays, and ultraviolet light (UV). UV is divided into A, B, and C, depending on the wavelength and increases the risk of cancer [1]. UV penetrates deeper into the skin as the wavelength increases, and UVA and UVB damage the skin [2]. SSBs and 8-OHdG are removed by base excision repair (BER). In BER, DNA damage recognized by DNA glycosylase such as monofunctional and bifunctional glycosylase [9]. Those increase the AP site by removing the damaged base and recruit AP endonuclease 1 and flap endonuclease 1 [10]. NER removes bulk DNA adducts by regulating the DNA excision repair genes [13]. DNA excision repair genes related to NER involve in growth arrest and DNA damage α (Gadd45α), p48-XPE, and DNA polymerase, which are regulated by p53 [17]

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