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Diosgenin (a steroidal saponin of yam) has long been used as a raw material for the industrial production of steroid drugs, and reported to have a hypocholesterolemic effect by suppressing cholesterol absorption and increasing cholesterol secretion. Oxidative stress has been suggested as a main risk factor in the development of atherosclerosis. The aim of this study is to investigate the possible hypolipidemic and antioxidative effect of diosgenin on rats fed with a high-cholesterol diet supplemented with either 0.1% or 0.5% diosgenin for 6 weeks. We measured the lipid profile in the plasma and liver, lipid peroxidation and antioxidative enzyme activities in the plasma, erythrocyte and gene expression of antioxidative enzymes in the liver, and the oxidative DNA damage in lymphocytes. Diosgenin showed a decrease in the plasma and hepatic total cholesterol levels, but increased the plasma high-density lipoprotein (HDL) cholesterol level. Erythrocyte TBARS and lymphocyte DNA damage measured by the comet assay were decreased in the diosgenin supplemented group. Furthermore, diosgenin feeding enhanced the resistance to lymphocyte DNA damage caused by an oxidant challenge with H(2)O(2). The antioxidative enzyme activities were also affected by diosgenin supplementation. Total superoxide dismutase (SOD) in the plasma and liver, glutathione peroxidase (GSH-Px) in erythrocytes, and catalase (CAT) in erythrocytes and liver were significantly increased in the 0.5% diosgenin group. The expression of antioxidative enzymes was up-regulated by diosgenin, the expression of GSH-Px being the highest in the 0.5% diosgenin group. These results suggest that diosgenin could be a very useful compound to control hypercholesterolemia by both improving the lipid profile and modulating oxidative stress.

In the process of screening for pancreatic lipase inhibitors, which could be used as an anti-obesity measure, the methanol extract of Dioscorea nipponica Makino powder (DP) appeared to have potent inhibitory activity against porcine pancreatic lipase with an IC50 value of 5-10 microg/ml, where the enzyme activity was assayed by using 4-methylumbelliferyl oleate as a substrate. Further purification of active components present in the herb generated dioscin that belongs to the saponin family. Dioscin and its aglycone, diosgenin, both suppressed the time-dependent increase of blood triacylglycerol level when orally injected with corn oil to mice, suggesting their inhibitory potential against fat absorption. Sprague-Dawley rats fed on a high-fat diet containing 5% Dioscorea nipponica Makino and 40% beef tallow gained significantly less body weight and adipose tissue than control animals fed on a high-fat diet alone during an 8-week experimental period (P<0.05).

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The zinc nutritional status in south Koreans was established by evaluation of zinc, calcium and phytate intakes, the molar ratio of phytate:zinc, and the millimolar ratio of phytate x calcium:zinc. The intakes of iron and magnesium were also estimated. Sampling was designed so that it was representative of the national population. Two-day food records were used for the calculation of nutrient intakes, using food consumption data from the 1995 National Nutrition Survey ('95NNS) for South Korea. Daily intakes of zinc and calcium were estimated to be 10.1 mg/d and 426.5 mg/d, respectively, and those of iron and magnesium were 15.2 mg/d and 268.0 mg/d, respectively. The estimated daily phytate intake was 1676.6 mg/d. The ratio of phytate:zinc was 15.9 mol/d and that of phytate x calcium:zinc was 168.9 mmol/d. The ratio in millimoles per 4.2 MJ (1000 kcal) of phytate x calcium:zinc was 91.8. The major food groups for zinc intake were meat, poultry and their products (43%), and cereals and grain products (18%). Sixty-two percent of zinc was from animal food sources. Cereal and grain products supplied most of the phytate intake (46%) followed by seasonings, fruits, and legumes and their products. The major food source of phytate was rice (39%). The results of the study raise concern about the suboptimal zinc status in relation to the Western diet.

Papyriflavonol A (PapA), a prenylated flavonoid [5,7,3',4'tetrahydroxy-6,5'-di-(γ,γ-dimethylallyl)-flavonol], was isolated from the root barks of Broussonetia papyrifera. Our previous study showed that PapA has a broad-spectrum antimicrobial activity against pathogenic bacteria and fungi. In this study, the mode of action of PapA against Candida albicans was investigated to evaluate PapA as an antifungal agent. The minimal inhibitory concentration (MIC) values were 10~25 µg/ml for C. albicans and Saccharomyces cerevisiae, Gram-negative bacteria (Escherichia coli and Salmonella typhimurium), and Gram-positive bacteria (Staphylococcus epidermidis and Staphylococcus aureus). The kinetics of cell growth inhibition, scanning electron microscopy, and measurement of plasma membrane florescence anisotrophy revealed that the antifungal activity of PapA against C. albicans and S. cerevisiae is mediated by its ability to disrupt the cell membrane integrity. Compared with amphotericin B, a cell-membranedisrupting polyene antibiotic, the hemolytic toxicity of PapA was negligible. At 10~25 µg/ml of MIC levels for the tested strains, the hemolysis ratio of human erythrocytes was less than 5%. Our results suggest that PapA could be a therapeutic fungicidal agent having potential as a broad spectrum antimicrobial agent.

Glyceollins, which are derived from daidzein in soybean in response to various stimuli or stresses, have been reported to activate antioxidant/detoxifying enzymes in a nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-dependent manner, in addition to exerting anti-inflammatory effects in murine macrophages. As the Nrf2 signaling pathway is known to antagonize nuclear factor (NF)-κB signaling, glyceollins likely have the potential to prevent or treat inflammatory bowel disease. Thus, this study was conducted to examine whether glyceollins could inhibit dextran sulfate sodium (DSS)-induced colitis in a mouse model. Ulcerative colitis (UC) was induced in male BALB/c mice by administering drinking water with 4% DSS for 5 days. Glyceollins (4 or 10 mg/kg of body weight) were orally administered 48 h before and after DSS treatment. We found that glyceollins alleviated histological colon damage and inflammation induced by DSS treatment. More specifically, glyceollins reduced plasma levels of inflammatory cytokines, such as tumor necrosis factor-α and interleukin-6, which were otherwise markedly increased by DSS treatment. Markers of tissue damage, including malondialdehyde and 8-hydroxy-2-guanosine, were significantly increased by DSS treatment; however, this effect was mitigated through concomitant treatment with glyceollins. Furthermore, nuclear accumulation of NF-κB p65 and the expression of inducible nitric oxide synthase were upregulated by glyceollins, consistent with the observed modulation of inflammatory markers. In conclusion, glyceollins have therapeutic potential for UC and merit further clinical study.