Protective effects of tacalcitol against oxidative damage in human epidermal melanocytes.

Autor: Li QL; Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China., Wu YH; Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China., Niu M; Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China., Lu XJ; Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China., Huang YH; Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China., He DH; Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China.
Jazyk: angličtina
Zdroj: International journal of dermatology [Int J Dermatol] 2017 Feb; Vol. 56 (2), pp. 232-238.
DOI: 10.1111/ijd.13407
Abstrakt: Background: Oxidative damage may lead to the dysfunction of melanocytes (MCs) and is one of the causative mechanisms involved in the pathogenesis of vitiligo.
Objectives: This study was designed to investigate the protective effects of the vitamin D3 analog tacalcitol on oxidative damage induced by hydrogen peroxide (H 2 O 2 ) in human epidermal MCs.
Methods: Human epidermal MCs were cultured and identified by l-DOPA staining and HMB-45 immunohistochemical staining. The model of oxidative damage induced by H 2 O 2 was established, and the cells were treated with tacalcitol. The viability of MCs was determined using an MTS assay. Morphological changes in cell dendrites were observed by microscopy, and the rate of change of dendrites was calculated. The reactive oxygen species (ROS) level in MCs was determined using immunofluorescence microscopy. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels in MCs were determined using the WST-1 and TBA methods, respectively.
Results: In comparison with the control group, the viability of MCs and SOD activity were significantly decreased in the H 2 O 2 group (P < 0.05) and significantly increased in the tacalcitol group (P < 0.05). In comparison with the control group, the rate of change of cell dendrites and levels of ROS and MDA were significantly increased in the H 2 O 2 group (P < 0.05) and significantly decreased in the tacalcitol group (P < 0.05).
Conclusions: Tacalcitol can reduce oxidative damage induced by H 2 O 2 in MCs by inhibiting intracellular ROS overproduction, increasing SOD activity, and decreasing the level of MDA, thereby reducing cell apoptosis.
(© 2017 The International Society of Dermatology.)
Databáze: MEDLINE
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