Naringin protects ultraviolet B-induced skin damage by regulating p38 MAPK signal pathway

• Naringin is known to have properties of free radical scavenging [10], inhibition of tumor growth [11] and anti-apoptosis [12].
• In this study, we found that naringin can resist UVB-induced skin damage by inhibiting ROS and inflammation reactions in vivo and in vitro.
• It can also prevent high COX-2 expression due to UV irradiation by inhibiting the activity of MAPK/p38 signal pathway.
• Our results indicate that naringin is likely to be an effective therapeutic agent providing protection against UVB-induced skin disorders.

BackgroundNaringin is a bioflavonoid and has free radical scavenging and anti-inflammatory properties.MethodsWe examined the effects of naringin on skin after ultraviolet radiation B (UVB) irradiation and the signal pathways by in vitro and in vivo assay.ResultsHaCaT cells pretreated with naringin significantly inhibited UVB induced-cell apoptosis and production of intracellular reactive oxygen species (ROS). The expressions of interleukin-1β (IL-1β), 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.ConclusionNaringin 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.