Abstract
Objective
Licoricidin 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).
Methods
In vitro ROS scavenging activity, cellular protective effect and inhibition of elastase activity was determined by Fe3+-EDTA/H2O2 systems, photohemolysis 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.
Results
The ROS scavenging activity (OSC50) of licoricidin was 2.77 μM. It was 3.1-fold higher than that of L-ascorbic acid. Its protective effects were confirmed in a study of 1O2-induced cellular damage to human erythrocytes. The τ50 value of 10 μM of licoricidin was 71.0 min; this was markedly higher than that obtained with α-tocopherol (37.0 min). The elastase inhibitory activity of licoricidin (IC50 of 61.2 μM) 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 MAPK phosphorylation, which resulted in decreased c-Jun activation and reduced c-Jun and c-Fos expression.
Conclusion
Licoricidin blocks UVA-induced photoaging via ROS scavenging. This activity converge to limit the activity of MMP-1. These data suggest that licoricidin may be considered as an active ingredient in new topically applied anti-aging formulations.
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