BVD protects against UVB-induced HaCaT keratinocytes photodamage through reactivating Nrf2 antioxidative stress signaling

Background : To investigate the protective role and mechanism of exogenous biliverdin (BVD) on ultraviolet B (UVB) irradiated human keratinocytes (HaCaT cells). Methods : Cultured HaCaT cells were divided into control group, UVB group, and BVD + UVB group. Morphological changes in the HaCaT cells were observed, the cell viability of each group was detected, the mean fluorescence intensity (reactive oxygen species, ROS) of the cells was detected, the superoxide dismutase (SOD) and malondialdehyde (MDA) levels of the cells were detected, and the protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), matrix metalloproteinase-1 (MMP-1), and matrix metalloproteinase-3 (MMP-3) were determined. Moreover, Nrf2 gene transfection was performed in HaCaT cells. Results : UVB irradiation induced apoptosis of HaCaT cells, decreased Nrf2 protein expression and increased MMP-1 and MMP-3 protein expression, which increased ROS and MDA levels and decreased SOD levels. Nrf2 gene enhancement increased UVB-irradiated HaCaT cell viability. Conclusion : Exogenous BVD plays a protective role in UVB-induced HaCaT cell damage, and this effect may be related to the Nrf2 antioxidant signaling pathway. Keywords : Biliverdin, UVB irradiation, Photo-damage，Nrf2，oxidativestress，HaCaT

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