Camellia japonica L. is a plant of which the seeds are used as a folk medicine, and it is native to South Korea, Japan and China. In previous study, triterpenes, flavonoids, tannins and fatty acids which have antiviral, antioxidant and anti inflammatory activity were reported from C. japonica leaf and flower. In Korea, the seed from this plant is used as a traditional medicine and in folk remedies for the treatment of bleeding and inflammation. However, the major issue associated with the use of the seed as a medicinal and/or functional food ingredient is its application to the pharmaceutical and food industry. First, the productivity of seed extract is very much less than that of the leaf. Second, the beneficial usage of the seed extract as an alternative medicine and functional source is not yet clear. Thus, in this study, we focused on another part of the plant, the leaf, and found that the extract of Camellia japonica leaf has a high concentration of vitamin E, rutin and other biologically active compounds related to hyperuricemia. We aimed to investigate the biological activities, namely the antioxidant activities, xanthine oxidase (XO) inhibitory activity and anti‑hyperuricemic effects of extract from C. japonica leaf and the phytochemicals contained therein. Ethanol extracts of C. japonica leaf (ECJL) were prepared, and the extract was used with respect to antioxidant activities, total phenolic contents and XO inhibitory activity. The in vivo XO inhibitory activity and anti‑hyperuricemic effects of the extract were evaluated in mice with potassium oxonate‑induced hyperuricemia. To clarify the marker compounds that are responsible for the anti‑hyperuricemic effects, several key constituents were identified using gas chromatography‑mass spectrometry (GC‑MS) and and liquid chromatography-mass spectrometry (LC-MS). ECJL was found to have strong antioxidant activities, and in vitro XO inhibitory activity. The results of the in vivo experiments using mice demonstrated that ECJL at the doses of 100 and 300 mg/kg inhibited hepatic XO activity and significantly attenuated hyperuricemia. To the best of our knowledge, the present study is the first report on the XO inhibitory and anti-hyperuricemic effects of ECJL, which can be therapeutically applied in the treatment of hyperuricemia and gout.

Asthma is a chronic respiratory disease related to hyper-responsiveness. The majority of patients suffer mild symptoms, however, some cases, especially in the young and the elderly, can lead to death by apnea. Mycoleptodonoides atichisonii (M. atichisonii) is an edible mushroom that has previously been reported to possess several bioactive properties, such as the synthesis of nerve growth factors, anti-obesity effects and the ability to prevent cell death. In the current study, the authors evaluated the anti-asthmatic effects of M. atichisonii using an ovalbumin-induced asthma mouse model. M. atichisonii dose-dependently suppressed the levels of white blood cells, eosinophils and immunoglobulin (Ig)E in BALB/c mice, resulting from ovalbumin-induced asthma. M. atichisonii recovered the typical asthmatic morphological changes in lungs, such as mucous hyper-secretion, epithelial layer hyperplasia, eosinophil infiltration and various cell surface molecules, such as CD3, CD4, CD8, CD19 and major histocompatibility complex class II. With the exception of CD19+ cells and IL-12p40, M. atichisonii affected almost all factors related to asthma induction including the T helper (Th)1/Th2 transcription factors, T-bet and GATA-3, Th1-related cytokines, Th2-related cytokines and proinflammatory cytokines. In addition, M. atichisonii significantly inhibited the expression of IL-5, IL-13 and IL-6. The authors concluded that M. atichisonii may be a promising drug candidate against asthma.

In 2013, WHO estimated that approximately 235 million people suffered from asthma worldwide. Asthma is a hyper responsive disorder, which is related to an imbalance between the T-helper type 1 and 2 cells (henceforth, Th1 and Th2, respectively). Allium hookeri is a plant that is widely used for culinary purposes and also in traditional Asian medicine. The present study was conducted to elucidate the anti-asthmatic effects and mechanism of action of A. hookeri root extracts (AHRE) in an ovalbumin (OVA)-induced asthma mouse model. The mice were divided into five groups, namely, the control, the OVA-treated group, the dexamethasone-treated group, the 30 mg/kg AHRE-treated group, and the 300 mg/kg AHRE-treated group. The total WBC count and the differential cell count in the bronchoalveolar fluid, the level of serum IgE, the histopathological changes in the lung, and changes in the cell surface molecules, the asthma-related cytokine levels, and Th cell transcription factors were evaluated. AHRE significantly ameliorated asthmatic changes, such as the total WBC count, eosinophil count, and the level of IgE; in addition, it reduced mucus hypersecretion, epithelial hyperplasia, and eosinophil infiltration in the lungs. AHRE significantly inhibited the expression of CD68+ cells and MHC class II+ molecules, Th1 cell transcription factor (T-bet) activation, Th2 cell transcription factor (GATA-3) activation, and TNF-α in the lung tissue. Furthermore, it suppressed cell surface molecules, such as CD4+and CD8+; Th1-related cytokines, such as IFN-γ and IL-12p40; Th2-related cytokines, such as IL-4 and IL-5; and Th17-related cytokines, such as IL-6 and TNF-α, in a dose-dependent manner. Thus, AHRE may be considered a promising anti-asthmatic drug.

Gallic acid (3, 4, 5‐trihydroxybenzoic acid) is a phytochemical derived from diverse herbs. It has been reported to have effective antifungal, antiviral and antioxidant activity. However, gallic acid exhibits low solubility and instability at high temperatures. In a previous study, in order to overcome these limitations, we synthesized galloyl‐RGD by combining gallic acid with arginine, glycine and asparaginic acid (RGD peptide). This compound showed better thermal stability than gallic acid. In this study, we investigated the antimelanogenic effect of galloyl‐RGD and the underlying mechanism for this effect. Galloyl‐RGD markedly inhibited melanin content and tyrosinase activity in a concentration‐dependent manner. We also found that galloyl‐RGD decreased the levels of melanogenesis‐related gene and protein. In addition, galloyl‐RGD reduces intracellular cyclic adenosine monophosphate (cAMP) levels that leads to inhibition of cAMP‐responsive element binding protein (CREB) phosphorylation and activates extracellular signal‐regulated kinase (ERK) expression. These results indicate that CREB and ERK regulation by galloyl‐RGD contributes to reduced melanin synthesis via degradation of microphthalmia‐associated transcription factor. Therefore, galloyl‐RGD can be potential candidate for application in cosmetic or pharmaceutical industry.