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

• Published in: Cutaneous and ocular toxicology Vol. 42; no. 2; p. 74
• Main Authors: Wang, Pingwei, Liu, Dongge, Cui, Jiajing, Yan, Shuqi, Liang, Yujun, Chen, Qianqian, Liu, Yanping, Ren, Shuping, Chen, Peng
• Format: Journal Article
• Language: English
• Published: England 03.04.2023
• Subjects: Apoptosis - radiation effects; bcl-2-Associated X Protein - metabolism; Beclin-1 - metabolism; Humans; Keratinocytes - metabolism; NF-kappa B - metabolism; Reactive Oxygen Species - metabolism; Ultraviolet Rays - adverse effects; UVB; ultraviolet radiation; skin; 125(OH)2D3; apoptosis; oxidative stress
• ISSN: 1556-9535
• DOI: 10.1080/15569527.2023.2208676

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) D ) 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) D 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) D used in the study was 100 nM and the UVB irradiation intensity was 20 mJ/cm . Compared with the HaCaT cells irradiated with UVB, the HaCaT cells that were pre-treated with 1,25(OH) D had lower production of ROS, lower expression of NF-κB, Caspase9, Caspase3, Bax, FADD, CytC and Beclin-1(  < 0.05). 1,25(OH) D 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.