Background : Black ginseng is known to be effective product made with ginseng. In general, most black ginseng is manufactured by high teperature condition (90 - 95℃). However this temperature condition may not be optimal to obtain ginsenoside components beneficial for inhibition of diabetes. Here, we examined anti-diabetic effect of black ginseng manufactured by low low temperature process. Methods and Results : For diabetes induction, ICR mice were intraperitoneally injected with alloxan (50 ㎎/㎏). Mice were administered orally with 1 or 3 ㎎/mouse of the extract of black ginseng (BG-L) manufactured with low temperature (80℃), and its anti-diabetic effect was evaluated by measuring the level of glucose in blood. The consecutive administration of BG-L extract resulted in a significant decrease of glucose. In oral and intravenous glucose tolerance test (OGTT and IVGTT, respectively), administration of BG extract significantly reduced the level of glucose in blood within 20 min after glucose treatment. And its suppressive effect on glucose tolerance was effective not only pre-treatment but also post-treatment of BG extract. Oral administration of BG extract enhanced the level of insulin in blood, and decreased the amount of water consumption in alloxan-induced diabetic mice 5 days after alloxan treatment. In addition, BG-L significantly inhibited the level of blood glucose in db/db type-II diabetic mice. Conclusion : These results suggest that the black ginseng extract manufactured manufactured with low temperature (80℃) is a promising candidate applicable to the development of anti-diabetic nutraceutical foods and drugs.

Background : Cudrania tricuspidata Bureau belonging to the mulberry family has attracted much attention as a nutrition ingredient many times as many as the mulberry tree. In this study, we examined the inhibitory effect of hot water extract of Cudrania tricuspidata Bureau fruits (CT-F) on inflammation and inflammatory diseases such as diabetes and gastiritis in cell-level experiments and animal models using mice. Methods and Results : The inhibitory effect of CT-F was investigated in LPS_stimulated RAW264.7 macrophages. Treatment with CT-F significantly inhibited the production of inflammatory mediators such as NO, IL-6 and TNF-a. The inhibitory effect of CT-F was shown to be related to inhibition of NF-kB activation in LPS-stimulated macrophages. In in vivo diabetic models using mice, treatment of CT-F lowered the level of blood glucose in alloxan-induce type-1 diabetic model as well as db/db type-2 mice model. CT-F also dramatically inhibited gastiritis induced by EtOH/HCl in mice. Conclusion : Hot water extract of Cudrania tricuspidata Bureau fruits was effective for inhibition of inflammation, diabetes and gastirits. Therefore, CT-F is thought to be a beneficial candidate for development of functional foods to prevent inflammation-associated diseases.

Anti-inflammatory activity of the extracts of ginseng berry (GBE) was investigated through the evaluation of its inhibitory effect on the production of inflammatory meditator, nitric oxide(NO), tumor necrocis factor-alpha (TNF-α), interleukin-6 (IL-6) in LPS-induced RAW264.7 macrophage cells. GBE was fractionated using n-hexane, chloroform, ethylacetate, buthanol and H2O, sequentially. RAW264.7 cells were induced 100ng/mℓ of lipopolysaccharide (LPS) and treated with 0, 1.6, 8, 40 and 200μg/mℓ of GBE fractions. LPS-induced NO production on all of GBE fractions was inhibited with increasing added concentration of GBE fractions. Chloroform fraction of GBE was the most effective in inhibiting LPS-induced TNF-α production. Hexane, chloroform and H2O fractions of GBE exhibit strong inhibition LPS-induced IL-6 production. Especially, H2O fractions of GBE was the most effective in inhibiting LPD-induced IL-6 production without significant cytotoxicity in RAW264.7 cells, and reduced the activation of mitogen-activated protein kinases (MAPK) and IkB phosphorylation. These results indicate that H2O fractions of GBE exhibits strong anti-inflammatory effects by inhibition of NF-kB by inhibition of p-38 on MAPK and IkB phosphorylation.