期刊
JOURNAL OF DERMATOLOGICAL SCIENCE
卷 82, 期 2, 页码 106-114出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jdermsci.2015.12.008
关键词
UVB; Naringin; COX-2; p38
类别
资金
- National Natural Science Foundation of China [81272226, 81301356]
- Key Science and Technology Projects from the Science and Technology Commission of Shanghai Municipality [13JC1405102]
Background: Naringin is a bioflavonoid and has free radical scavenging and anti-inflammatory properties. Methods: We examined the effects of naringin on skin after ultraviolet radiation B (UVB) irradiation and the signal pathways by in vitro and in vivo assay. Results: HaCaT cells pretreated with naringin significantly inhibited UVB induced-cell apoptosis and production of intracellular reactive oxygen species (ROS). The expressions of interleukin-1 beta (IL-1 beta) interleukin-6 (IL-6), interleukin-8 (IL-8) and cyclooxygenase-2 (COX-2) in HaCaT cells pretreated with naringin were decreased compared with the only UVB group. Also, the activation of p38 induced by UVB in HaCaT cells was reversed by naringin treatments. The inhibition function of naringin on p38 activity was more obvious than JNK. In vivo, topical treatments with naringin prevented the increase of epidermal thickness, IL-6 production, cell apoptosis and the overexpression of COX-2 in BALB/c mice skin irradiated with UVB. Naringin treatment also markedly blocked the activation of p38 in response to UVB stimulation in the mouse skin. Conclusion: Naringin can effectively protect against UVB-induced keratinocyte apoptosis and skin damage by inhibiting ROS production, COX-2 overexpression and strong inflammation reactions. It seemed that naringin played its role against UVB-induced skin damage through inhibition of mitogen-activated protein kinase (MAPK)/p38 activation. (C) 2016 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
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