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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) 2 D 3 ) will attenuate the damage of human immortalised keratinocytes (HaCaT) cells caused by UVB and relevant underlying mechanisms. CCK-8 was employed to determine the UVB irradiation intensity and 1,25(OH) 2 D 3  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. The concentration of 1,25(OH) 2 D 3  used in the study was 100 nM and the UVB irradiation intensity was 20 mJ/cm 2 . Compared with the HaCaT cells irradiated with UVB, the HaCaT cells that were pre-treated with 1,25(OH) 2 D 3  had lower production of ROS, lower expression of NF-κB, Caspase9, Caspase3, Bax, FADD, CytC and Beclin-1( P  &lt; 0.05). 1,25(OH) 2 D 3  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.

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