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; UVB; apoptosis; oxidative stress; skin; ultraviolet radiation.