NORIKO Minamisawa, MIAO Ming-San, KANG Le, LIU Hui-Juan, CUI Lin-Lin, HIROKI Kanemisu, TERUMI Naito, HIROAKI Shinotsuka. Protective Effects of Jin Bai Mei Yan Prescription on Oxidative Damage and Photoaging Induced by Ultraviolet B in HaCaT Cells[J]. Digital Chinese Medicine, 2020, 3(2): 57-66. DOI: 10.1016/j.dcmed.2020.06.001
Citation: NORIKO Minamisawa, MIAO Ming-San, KANG Le, LIU Hui-Juan, CUI Lin-Lin, HIROKI Kanemisu, TERUMI Naito, HIROAKI Shinotsuka. Protective Effects of Jin Bai Mei Yan Prescription on Oxidative Damage and Photoaging Induced by Ultraviolet B in HaCaT Cells[J]. Digital Chinese Medicine, 2020, 3(2): 57-66. DOI: 10.1016/j.dcmed.2020.06.001

Protective Effects of Jin Bai Mei Yan Prescription on Oxidative Damage and Photoaging Induced by Ultraviolet B in HaCaT Cells

  • ObjectiveUltraviolet B (UVB) mainly acts on the skin epidermis, causing oxidative damage and apoptosis of keratinocytes. Jin Bai Mei Yan Prescription (JBMYP) comprises a variety of antioxidant traditional Chinese medicines (TCM). In this study, we aimed to evaluate the effects of JBMYP on the oxidative damage induced by UVB in human immortalized epidermal keratinocytes (HaCaT) cells.
    MethodsHaCaT cells were divided into six groups: control group, model (UVB) group, positive (UVB + vitamin E) group, UVB + JBMYP low dose group (160 μg/mL), UVB + JBMYP mode-rate dose group (800 μg/mL), and UVB + JBMYP high dose group (1 600 μg/mL). HaCaT cells were irradiated with UVB and treated with JBMYP for 24 h. Methyl thiazolyl tetrazolium (MTT) assay and real-time unlabeled cell function analyzer were used to assess the cell survival and proliferation rates, respectively. At the same time, the levels of intracellular reactive oxygen species (ROS), lipid peroxide malondialdehyde (MDA), glutathione (GSH), and hydroxyproline (HYP), as well as the activities of antioxidant enzyme superoxide dismutase (SOD) and catalase (CAT) were evaluated using enzyme linked immunosorbent assay (ELISA).
    ResultsCompared with the model group, the survival rate of HaCaT cells in each dosage group of JBMYP was significantly improved (P < 0.05). Further, JBMYP could promote the proliferation of HaCaT cells, leading to a reduction in the contents of MDA and ROS, and increase in the contents of SOD, CAT, GSH and HYP in HaCaT cells.
    ConclusionsJBMYP has enhanced protective effect on oxidative damage induced by UVB in HaCaT cells.
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