| In vitro: |
| Int J Mol Sci. 2016 Jun 14;17(6). pii: E934 | | Licoricidin, an Active Compound in the Hexane/Ethanol Extract of Glycyrrhiza uralensis, Inhibits Lung Metastasis of 4T1 Murine Mammary Carcinoma Cells[Pubmed: 27314329 ] | Licorice extracts containing glycyrrhizin exhibit anti-carcinogenic properties. Because glycyrrhizin induces severe hypokalemia and hypertension, we prepared a hexane/ethanol extract of Glycyrrhiza uralensis (HEGU) that lacks glycyrrhizin, and showed that HEGU induces apoptosis and G1 cell cycle arrest and inhibits migration of DU145 human prostate cancer cells. Our previous in vitro studies identified two active components in HEGU: isoangustone A, which induces apoptosis and G1 cycle arrest, and Licoricidin, which inhibits metastasis.
METHODS AND RESULTS:
This study examined whether HEGU and Licoricidin inhibit metastasis using the 4T1 mammary cancer model. Both HEGU and Licoricidin treatment reduced pulmonary metastasis and the expression of CD45, CD31, HIF-1α, iNOS, COX-2, and VEGF-A in tumor tissues. Additionally, a decrease in protein expression of VEGF-R2, VEGF-C, VEGF-R3, and LYVE-1 was noted in tumor tissues of Licoricidin-treated mice. Furthermore, the blood concentrations of MMP-9, ICAM-1, VCAM-1, and VEGF-A were decreased in HEGU-treated mice. In vitro 4T1 cell culture results showed that both HEGU and Licoricidin inhibited cell migration, MMP-9 secretion, and VCAM expression.
CONCLUSIONS:
The present study demonstrates that the Licoricidin in HEGU inhibits lung metastasis of 4T1 mammary carcinoma cells, which may be mediated via inhibition of cancer cell migration, tumor angiogenesis, and lymphangiogenesis. | | Int J Cosmet Sci. 2017 Apr;39(2):133-140. | | Licoricidin, an isoflavonoid isolated from Glycyrrhiza uralensis Fisher, prevents UVA-induced photoaging of human dermal fibroblasts.[Pubmed: 27502959 ] | 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 AND RESULTS:
In vitro reactive oxygen species (ROS) scavenging activity, cellular protective effect and inhibition of elastase activity was determined by Fe3+ -EDTA/H2 O2 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.
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 1 O2 -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 mitogen-activated protein kinases (MAPK) phosphorylation, which resulted in decreased c-Jun activation and reduced c-Jun and c-Fos expression.
CONCLUSIONS:
Licoricidin 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. | | J Breath Res. 2012 Mar;6(1):016006 | | Reduction of bacterial volatile sulfur compound production by licoricidin and licorisoflavan A from licorice.[Pubmed: 22368239 ] | Halitosis affects a large proportion of the population and is, in most cases, caused by the production of volatile sulfur compounds (VSCs), particularly methyl mercaptan and hydrogen sulfide, by specific bacterial species colonizing the oral cavity.
METHODS AND RESULTS:
In this study, a supercritical extract of Chinese licorice (Glycyrrhiza uralensis), and its major isoflavans, Licoricidin and licorisoflavan A, were investigated for their effect on growth, VSC production and protease activity of Porphyromonas gingivalis, Prevotella intermedia and Solobacterium moorei, which have been associated with halitosis. The effects of licorice extract, Licoricidin, and licorisoflavan A on VSC production in a saliva model were also tested. We first showed that Licoricidin and licorisoflavan A, and to a lesser extent the licorice extract, were effective in inhibiting the growth of all three bacterial species, with minimal inhibitory concentrations in the range of 2-80 μg ml(-1).
CONCLUSIONS:
Within the limitations of this study, it can be concluded that a licorice supercritical extract and its major isoflavans (Licoricidin and licorisoflavan A) represent natural ingredients with a potential for reducing bacterial VSC production and therefore for controlling halitosis. | | Chem Biol Interact . 2018 Jun 25;290:44-51. | | Licoricidin enhances gemcitabine-induced cytotoxicity in osteosarcoma cells by suppressing the Akt and NF-κB signal pathways[Pubmed: 29782821] | | Abstract
Osteosarcoma (OS) is the most common bone malignancy in children and adolescents. Combined treatments of anti-cancer drugs can remarkably improve chemotherapeutic outcomes. Gemcitabine and Licoricidin both have potential anti-tumor activity in several cancers. However, the combined therapeutic efficiency of gemcitabine and Licoricidin for OS has not been explored. Here, we found that Licoricidin or gemcitabine inhibited OS cell viability in a dose-dependent manner. Cotreatment with Licoricidin and gemcitabine enhanced gemcitabine-induced cytotoxicity in OS cells. Licoricidin suppressed activation of the Akt and nuclear factor-kappa B (NF-κB) pathways. Gemcitabine had no effect on Akt signal, but facilitated the activation of NF-κB signal in OS cells. Moreover, combined treatment of Licoricidin and gemcitabine markedly curbed the activation of Akt and NF-κB pathways in OS cells. Inhibition of the Akt and NF-κB pathways enhanced gemcitabine-induced cytotoxicity in OS cells. In vivo assay further manifested that Licoricidin enhanced gemcitabine-induced cytotoxicity in tumor xenograft models of OS via inactivation of the Akt and NF-κB pathways. In conclusion, Licoricidin enhanced gemcitabine-induced cytotoxicity in OS cells by inactivation of the Akt and NF-κB pathways in vitro and in vivo.
Keywords: Gemcitabine; Licoricidin; Osteosarcoma. | | Int J Cosmet Sci . 2017 Apr;39(2):133-140. | | Licoricidin, an isoflavonoid isolated from Glycyrrhiza uralensis Fisher, prevents UVA-induced photoaging of human dermal fibroblasts[Pubmed: 27502959] | | 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 reactive oxygen species (ROS) scavenging activity, cellular protective effect and inhibition of elastase activity was determined by Fe3+ -EDTA/H2 O2 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.
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 1 O2 -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 mitogen-activated protein kinases (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 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.
Keywords: activator protein 1; Licoricidin; matrix metalloproteinases; mitogen-activated protein kinases; reactive oxygen species; ultraviolet A. |
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