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Glycyrrhizinic acid (GA), a principal component derived from licorice which is used extensively as a natural sweetener and traditional folk herbal medicine, is attracting considerable attention because of its broad range of bioactivities. However, the anti-inflammatory mechanism of GA on 12- O -tetradecanoylphorbol-13-acetate (TPA)-mediated skin inflammation has not been elucidated. Herein, we investigated the anti-inflammatory activity of GA by using a TPA-induced mouse ear model. It was indicated that GA, applied topically onto mouse ears, effectively inhibited the TPA-mediated expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner, respectively. Mechanistic investigations demonstrated that GA down-regulated the expressions of IκBα and p65 and blocked the phosphorylation of IκBα and p65 in TPA-induced mouse skin. Moreover, GA significantly inhibited the TPA-mediated activation of extracellular signal-regulated kinase (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI3K)/Akt, which are upstream of nuclear factor-kB (NF-κB). Taken together, these results indicated that GA, being of natural origin, may be a potential agent for preventing inflammatory diseases.

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Glycyrrhizic acid from licorice down-regulates inflammatory responses <i>via</i> blocking MAPK and PI3K/Akt-dependent NF-κB signalling pathways in TPA-induced skin inflammation

Glycyrrhizic acid from licorice down-regulates inflammatory responses via blocking MAPK and PI3K/Akt-dependent NF-κB signalling pathways in TPA-induced skin inflammation