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Abstract
Objective
Ultraviolet-B (UVB) radiation is an important factor in causing skin damage. The study is to explore whether 1,25-Dihydroxvitamin D3(1,25(OH)2D3) will attenuate the damage of human immortalised keratinocytes (HaCaT) cells caused by UVB and relevant underlying mechanisms.
Methods
CCK-8 was employed to determine the UVB irradiation intensity and 1,25(OH)2D3 concentration. Western blot was used to detect the expression of NF-κB, Caspase9, Caspase3, Bax, Bcl2, FADD, CytC, Beclin-1; Flowcytometry was applied to measure the production of ROS.
Results
The concentration of 1,25(OH)2D3 used in the study was 100 nM and the UVB irradiation intensity was 20 mJ/cm2. Compared with the HaCaT cells irradiated with UVB, the HaCaT cells that were pre-treated with 1,25(OH)2D3 had lower production of ROS, lower expression of NF-κB, Caspase9, Caspase3, Bax, FADD, CytC and Beclin-1(P < 0.05).
Conclusion
1,25(OH)2D3 could inhibit the development of oxidative stress and apoptosis in HaCaTs triggered by UVB. This inhibition might be achieved through the suppression of mitochondria-modulated apoptosis and autophagy. Vitamin D may be a potential UVB protective component.
Acknowledgements
We sincerely thank Associate Professor Yanan Shen of the Key Laboratory of Radiobiology of the National Health Care Commission for the gift of HaCaT cells to us.
Ethical standards
The manuscript does not contain clinical studies or patient data.
Author contributions
WP and LD conducted the experiment of this study. WP and LD collected the articles' data and drafted the manuscript. CJ, YS, LY, CQ, LY, CP, LH and RS contributed to the discussion and revision. CP is the corresponding author for this article. All authors read and approved the final manuscript.
Disclosure statement
No potential conflict of interest was reported by the authors.