Licoricidin, an isoflavonoid isolated from Glycyrrhiza uralensis Fisher, prevents UVA-induced photoaging of human dermal fibroblasts

ObjectiveLicoricidin is an isoflavonoid isolated from Glycyrrhiza uralensis Fisher. In this study, we investigated the effects of licoricidin on photoaging of UVA-irradiated human dermal fibroblasts (HDFs). MethodsIn vitro reactive oxygen species (ROS) scavenging activity, cellular protective effect and inhibition of elastase activity was determined by Fe3+-EDTA/H2O2 systems, photohaemolysis and elastase activity assay, respectively. Anti-oxidative capacity of the compound was evaluated by fluorescent ELISA and 2, 7-dichlorofluorescin-diacetate (DCF-DA) assay. The expression of protein and phosphorylation was examined using Western blot. ResultsThe ROS scavenging activity (OSC50) of licoricidin was 2.77 M. It was 3.1-fold higher than that of L-ascorbic acid. Its protective effects were confirmed in a study of O-1(2)-induced cellular damage to human erythrocytes. The (50) value of 10 M of licoricidin was 71.0 min; this was markedly higher than that obtained with -tocopherol (37.0 min). The elastase inhibitory activity of licoricidin (IC50 of 61.2 M) was 2.1-fold more potent than that of oleanolic acid. Licoricidin markedly reduced the UVA-induced intracellular ROS in a concentration-dependent manner. Western blot revealed that licoricidin attenuated the UVA-dependent induction of MMP-1 protein. Mechanistically, this appeared to be due to licoricidin-dependent inhibition of mitogen-activated protein kinases (MAPK) phosphorylation, which resulted in decreased c-Jun activation and reduced c-Jun and c-Fos expression. ConclusionLicoricidin blocks UVA-induced photoaging via ROS scavenging. This activity converges to limit the activity of MMP-1. These data suggest that licoricidin may be considered as an active ingredient in new topically applied anti-ageing formulations. Resume ObjectifLicoricidin est un isoflavonoide isole de Glycyrrhiza Fisher. Dans cette etude, nous avons etudie les effets de licoricidin sur le photovieillissement des fibroblastes dermiques humains UVA-irradies (HDFS). MethodeL'activite in vitro de piegeage des ROS, l'effet protecteur cellulaire et l'inhibition de l'activite de l'elastase ont ete determinees par des systemes de Fe3+ -EDTA / H2O2, par photohemolyse et par dosage de l'activite de l'elastase, respectivement. La capacite anti-oxydante du compose a ete evaluee par ELISA fluorescent et dosage du 2 , 7'-dichlorofluorescin-diacetate (DCF-DA). L'expression de la proteine et la phosphorylation ont ete examinees en utilisant Western Blot. ResultatsLa capacite antioxydante totale (OSC50) de licoricidin etait de 2,77 M. Il etait de 3,1 fois plus elevee que celle de l'acide L-ascorbique. Ses effets protecteurs ont ete confirmes dans une etude des dommages cellulaires O-1(2)- induite par les erythrocytes humains. La valeur 50 de 10 M de licoricidin etait de 71,0 min; ceci est nettement plus eleve que celle obtenue avec les -tocopherol (37,0 min). L'activite inhibitrice de l'elastase de licoricidin (CI50 de 61,2 M) etait de 2,1 fois plus puissante que celle de l'acide oleanolique. Licoricidin reduit nettement les ROS intracellulaires induits par les UVA d'une maniere dependante de la concentration. Western blot a montre que licoricidin attenue l'induction UVA-dependante de la proteine MMP-1. Du point de vue mecanistique, ceci semblait etre due a l'inhibition licoricidin dependante de la phosphorylation de MAPK, ce qui a entraine une diminution de l'activation de c-Jun et c-Jun reduite et l'expression de c-Fos. ConclusionLa licoricidin bloque le vieillissement entraine par les UVA par un captage des ROS. Cette activite converge pour limiter l'activite de MMP-1. Ces donnees suggerent que licoricidin devraient etre consideree comme un ingredient actif dans de nouvelles formulations anti-vieillissement appliquees par voie topique.