Abstract: Hu Wenzhi *, Ma Lijuan, Zhao Guang. *Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China Corresponding author: Zhao Guang, Email: guangfen@yahoo.com 【Abstract】 Objective To evaluate the effect of heat treatment on ultraviolet B （UVB）-induced oxidative injury to human melanocytes. Methods Melanocytes were isolated from adult foreskins, and subjected to a primary culture. After 3 － 4 passages of subculture, the melanocytes were classified into 4 groups: control group incubated at 37 ℃, heat treatment group incubated at 42 ℃ for 1 hour, UVB group exposed to UVB irradiation at 100 mJ/cm2, combination group receiving heat treatment at 42 ℃ for 1 hour followed by UVB irradiation at 100 mJ/cm2. After three successive days of treatment, MTT assay was performed to evaluate cell viability, a biochemical method to determine the activity of superoxide dismutase （SOD） and concentration of malonaldehyde （MDA）, and flow cytometry to detect intracellular reactive oxygen species （ROS） and apoptosis in melanocytes. Results The cell survival rate, apoptosis rate, SOD activity, MDA concentration and ROS level were （100 ± 6.14）%, （4.66 ± 0.58）%, （53.39 ± 8.23） U/gprot, （1.09 ± 0.32） mmol/gprot, and 1070.85 ± 42.07 in the control group respectively. UVB exposure induced a significant increase in apoptosis rate （24.14% ± 2.90%, P < 0.001）, MDA concentration （1.65 ± 0.33 mmol/gprot, P < 0.01） and ROS level （1416.45 ± 79.12, P < 0.01）, but a significant decrease in cell survival rate （50.23% ± 5.36%, P < 0.01） and SOD activity （31.98 ± 11.89 U/gprot, P < 0.01） in the UVB group compared with the control group, while the heat pretreatment markedly downregulated the UVB-induced increase in apoptosis rate （14.9% ± 1.49%, P < 0.001）, MDA concentration （1.10 ± 0.26 mmol/gprot） and ROS level （1033.30 ± 68.41, P < 0.01）, as well as the decrease in cell survival rate （ 74.12% ± 6.17%, P < 0.01） and SOD activity （51.63 ± 6.55 U/gprot, P < 0.01） in the combination group. Conclusion Heat treatment could protect melanocytes from UVB-induced oxidative injury.

Key words: Melanocytes, Heat, UVB, Oxidative stress