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Ginseng has been traditionally used for several millennia in Asian countries, including Korea, China, and Japan, not only as a nourishing and tonifying agent but also as a therapeutic agent for a variety of diseases. In recent years, the various effects of red ginseng including immunity improvement, fatigue relief, memory improvement, blood circulation improvement, antioxidation, mitigation of menopausal women's symptoms, and anticancer an effect have been reported in clinical as well as basic research. Around the world, there is a trend of the rising consumption of health functional foods on the level of disease prevention along with increased interest in maintaining health because of population aging and the awareness of lifestyle diseases and chronic diseases. Red ginseng occupies an important position as a health functional food. But till now, international ginseng monographs including those of the World Health Organization have been based on data on white ginseng and have mentioned red ginseng only partly. Therefore, the red ginseng monograph is needed for component of red ginseng, functionality certified as a health functional food in the Korea Food and Drug Administration, major efficacy, action mechanism, and safety. The present red ginseng monograph will contribute to providing accurate information on red ginseng to agencies, businesses, and consumers both in South Korea and abroad. Keywords: Health functional foods, Red ginseng, Red ginseng monograph

This study aimed to investigate the effect of apigenin, a flavonoid widely distributed in plants, on AK23-induced desmoglein3 (Dsg3) depletion in pemphigus vulgaris (PV) model using HaCaT cells. Dispase-based dissociation assay showed that the number of cell fragments, which increased compared to the control group due to AK23 treatment, dramatically decreased when HaCaT cells were incubated with AK23 and apigenin. The continuous linear fluorescence intensity of Dsg3 between cells was decreased in the AK23 group, but the treatment of apigenin recovered the fluorescent distribution of Dsg3. Moreover, the addition of apigenin up-regulated the Dsg3 protein expression in AK23-treated HaCaT cells. The phosphorylation level of p38 mitogen-activated protein kinase (MAPK) induced by the AK23 was down-regulated by apigenin. In conclusion, apigenin attenuated AK23-mediated Dsg3 depletion by suppressing the p38 pathway in the PV cell model. Therefore, apigenin could be a functional food material for ameliorating PV.

A biochip assay provides high-throughput and multiplexed analysis of biological samples, chemicals, and natural products. Pruritus is itchiness due to several causes, such as allergy, dry skin, pregnancy, liver disease, kidney disease, and thyroid disease. Treatment of pruritus is associated with reduced immunoglobulin (IgE) and FcεRI levels in sera. Treatment of pruritus include corticosteroid creams or ointment. However, they have side effects, so we need a safer treatment using natural products. Here, we developed an assay using protein chip technology to identify natural products with antipruritic activity that inhibit IgE-FcεRI binding. Of the 28 tested natural product extracts, Corni Fructus extract inhibited human IgE-FcεRI binding and also showed anti-histamine effects in MC/9 mast cells. These results suggest that this protein biochip assay system can be used to identify promising natural product extracts for the treatment of pruritus.

Elevated plasma LDL cholesterol is the dominant risk factor for the development of atherosclerosis and cardiovascular disease. Deficiency in the LDL receptor (LDLR) is a major cause of familial hypercholesterolemia in humans, and the LDLR knockout mouse is a major animal model of atherosclerosis. Here we report the generation and characterization of an ldlr mutant zebrafish as a new animal model to study hypercholesterolemia and vascular lipid accumulation, an early event in the development of human atherosclerosis. The ldlr mutant zebrafish were characterized by activated SREBP-2 pathway and developed moderate hypercholesterolemia when fed a normal diet. However, a short-term, 5-day feeding of ldlr mutant larvae with a high-cholesterol diet (HCD) resulted in exacerbated hypercholesterolemia and accumulation of vascular lipid deposits. Lomitapide, an inhibitor of apoB lipoprotein secretion, but not the antioxidant probucol, significantly reduced accumulation of vascular lipid deposits in HCD-fed ldlr mutant larvae. Furthermore, ldlr mutants were defective in hepatic clearance of lipopolysaccharides, resulting in reduced survival. Taken together, our data suggest that the ldlr knockout zebra­fish is a versatile model for studying the function of the LDL receptor, hypercholesterolemia, and related vascular pathology in the context of early atherosclerosis.—

Background: The loss of retinal pericytes is one of the earliest changes associated with diabetic retinopathy (DR). Chronic hyperglycemia induces apoptosis of these cells, leading to the onset and progression of DR. In this study, we investigated the effects of Homonoia riparia (H. riparia) and its major component, myricitrin, on high glucose (HG)-induced apoptosis of primary human retinal pericytes (HRPs). Methods: The effects of an ethanol extract of H. riparia leaves and of myricitrin on HRP viability and apoptosis were investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Reactive oxygen species (ROS) levels were measured using 2′,7′-dichlorofluorescein diacetate. The activity of specificity protein 1 (Sp1), a transcription factor, was measured using a luciferase reporter assay and western blot analyses were performed to measure the expression of proteins involved in signaling and apoptosis. Results: HG produced cytotoxic effects on HRPs, which showed increased Sp1 expression and ROS levels. H. riparia extract and myricitrin significantly inhibited HG-induced apoptosis and ROS generation, and also inhibited Sp1 activity. This was evidenced by an attenuation of the HG-mediated increase in extracellular signal-regulated kinase phosphorylation. Conclusion: These data indicate that HG-mediated induction of Sp1 is one of a number of key signaling pathways involved in HRP apoptosis, and that H. riparia extracts or myricitrin may provide useful approaches to preventing and treating DR.