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.

Acanthopanax trifoliatus (L.) Merr., an edible medicinal plant from Southeast Asia, exerts a wide range of bioactivities, such as anti-inflammatory activity. However, the anti-inflammatory mechanisms of its action and active constituents remain unclear. Herein, the effects of two triterpenoids, namely impressic acid (IA) and acankoreanogenin A (AA), from A. trifoliatus in both in vitro and in vivo chronic inflammation models were investigated. The results indicated that AA and IA reduced lipopolysaccharide (LPS)-induced production of nitroxide significantly in murine macrophage RAW246.7 cells. In addition, AA and IA down-regulated the activation of NF-κB and decreased the release of inflammatory mediators (iNOS, COX-2, TNF-α, and IL-6) and tumorigenesis-associated factors (MMP-9 and VEGF) in RAW246.7 cells. Furthermore, in a tetradecanoylphorbolacetate (TPA)-treated mouse model, AA and IA could effectively attenuate mouse ear edema and pathological damage and reduced levels of cytokines including iNOS, COX-2, TNF-α, and IL-1β. Taken together, AA and IA, being of natural origin, are promising anti-inflammatory agents and may contribute to the overall anti-inflammatory effect of A. trifoliatus.

Background: Essential oils (EOs), derived from aromatic plants, exhibit properties beneficial to health, such as anti-inflammatory, anti-oxidative, antidiabetic, and antiaging effects. However, the effect of EOs and their interaction in binary combinations against tyrosinase is not yet known. Objective: To evaluate the underlying mechanisms of EOs and their interaction in binary combinations against tyrosinas. Design: We explored to investigate the inhibitory effect of 65 EOs and the interaction among cinnamon, bay, and magnolia officinalis in their binary combinations against tyrosinase. In addition, the main constituents of cinnamon, bay, and magnolia officinalis were analyzed by gas chromatography–mass spectrometry (GC–MS). Results: The results showed that the most potent EOs against tyrosinase were cinnamon, bay, and magnolia officinalis with IC50 values of 25.7, 30.8, and 61.9 μg/mL, respectively. Moreover, the inhibitory mechanism and kinetics studies revealed that cinnamon and bay were reversible and competitive-type inhibitors, and magnolia officinalis was a reversible and mixed-type inhibitor. In addition, these results, assessed in mixtures of three binary combinations, indicated that the combination of cinnamon with bay at different dose and at dose ratio had a strong antagonistic effect against tyrosinase. Magnolia officinalis combined with cinnamon or bay experienced both antagonistic and synergistic effect in anti-tyrosinase activity. Conclusion: It is revealed that natural EOs would be promising to be effective anti-tyrosinase agents, and binary combinations of cinnamon, bay, and magnolia officinalis might not have synergistic effects on tyrosinase under certain condition.

Harmane, a compound derived from Peganum harmala L., was discovered as a lipid accumulation inhibitor with our triglyceride (TG) assay. To investigate the molecular mechanism underlying the role of harmane in the prevention of lipid accumulation, a number of biological experiments have been designed to determine if harmane reduces lipid accumulation by suppressing adipogenesis, lipogenesis, and regulating a specific signal transduction pathway. Our experimental data show that harmane inhibits TG accumulation though down-regulating the expression of adipogenic and lipogenic factors, up-regulating adipocyte browning markers and activating the SIRT1-LKB1-AMPK pathway. Therefore, harmane ameliorates obesity though inhibiting lipid accumulation and inducing adipocyte browning.

Tolfenamic acid (TA) and glycyrrhizic acid (GA) are well-known components with anti-inflammatory properties. However, their combined effects on inflammation have not been well studied. The present study aimed to investigate the in vivo anti-inflammatory effects of TA combined with GA using a 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear edema model, as well as the underlying mechanisms thereof. The results indicated that TA combined with GA led to a stronger inhibition on TPA-induced mouse ear edema compared to the singular treatments. In addition, the combined treatment significantly alleviated subcutaneous tissue inflammation caused by TPA. Further mechanistic investigations demonstrated that TA combined with GA decreased the levels of TPA-induced interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Furthermore, the combined treatment effectively inhibited nuclear factor-κB (NF-κB), extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK), phosphor-ERK1/2 and phosphor-JNK, which was accompanied by blocking of the activation and the phosphorylation in mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Akt signaling pathways. Collectively, our findings revealed that different anti-inflammatory components used in combination lead to enhanced inhibitory effects against inflammation.