1,25-Dihydroxvitamin D3 attenuates the damage of human immortalised keratinocytes caused by Ultraviolet-B

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.

Keywords:

• 125(OH)₂D₃
• skin
• ultraviolet radiation
• UVB
• oxidative stress
• apoptosis

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.

Additional information

Funding

We would like thank the Department of Science and Technology of Jilin Province for the financial support (Grant No. 20210204024YY).