• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.6
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• pp.1134-1141
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• 2002

Adhesion of leukocytes to the activated vascular endothelium and their subsequent recruitment/migration into the artery wall are key features in the pathogenesis of atherosclerosis and inflammatory diseases. These features have been mediated by cell adhesion molecules including vascular cell adhesion molecule-1 (VCAM-1) and in tracellular cell adhesion molecule-1 (ICAM-1). This study examined whether flavonoids inhibit the pro-inflammatory cytokine TNF-$\alpha$-induced monocyte adhesion via a modulation of the protein expression of VCAM-1 and ICAM-1 of human umbilical vein endothelial cells (HUVECs). TNF-$\alpha$ markedly increased the adhesion of THP-1 monocytes to endothelial cells and induced the expression of VCAM-1, ICAM-1 and E-selectin proteins in HUVECs. Micromolar concentrations of the flavones luteolin and apigenin and the flavonol quercetin near completely blocked the monocyte adhesion to the activated endothelial cells and the induction of these adhesion molecules. However, equimicromolar catechins of (-)epigallocatechin gallate and (+)catechin, the flavonol myr- icetin and the flavanones of naringin and hesperidin had no effect on TNF-$\alpha$-activated monocyte adhesion. (-)Epigallocatechin gallate, (+) catechin, and naringin did not attenuate the TNF-$\alpha$ induction of these adhesion molecules. Furthermore, culture with luteolin and apigenin strongly blocked the expression of TNF-$\alpha$-induced VCAM-1 mRNA and modestly attenuated ICAM-1 mRNA. Quercetin modestly decreased the TNF-$\alpha$-activated VCAM-1 and ICAM-1 mRNAs. These results demonstrate that flavonoids classified as flavones and flavonols may inhibit monocyte adhesion to the TNF-$\alpha$-activated endothelium, most likely due to a blockade of expression of functional adhesion molecules down-regulated at the transcriptional level, indicating a definite linkage between the chemical structure of flavonoids and the expression of cell adhesion molecules. Furthermore, the antiathero-genic feature of flavonoids appears to be independent of their antioxidant activity.

• Proceedings of the Ginseng society Conference
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• 1984.09a
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• pp.13-19
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• 1984

In the previous symposium, authors reported about anti-atherogenic action of Panax ginseng, saying that red-ginseng powder increased serum HDL-cholesterol, decreased total cholesterol, TG, NEFA, in addition, decreased platelet adhesiveness. Later, Toyama group including me. reported that ginsenosides esp. $Rb_2$ enhanced HDL and decreased LDL. Also Matsuyama group and Kinki Univ. group reported that ginsenosides $Rg_1,\;Rb_2,$ etc. inhibited platelet aggregation. This paper will be divided into two parts: Experimental and clinical Experimental study; Using a highcholesterol-cholic acid-fed rats, effects of red ginseng extract and several ginsenosides on serum apoprotein-lipoproteins in relation to prostaglandins. Rats received $2\%$ cholesterol 1-1$\%$ cholic acid diet, ginseng extract or ginsenosides 2.5mg/100g/day for 9 days. Red ginseng extract, ginsenosides $Rb_2,\;Rc,\;Rb_1,\;and\;Rg_1,\;esp.\;Rb_2,$ increased HDL, apo-AI, Aii and $PGI_2,$ while they decreased LDL, apo-B and $TXA_2$. Clinical study: Effect of red ginseng powder on hyperlipidemia was observed. Long term administration of red ginseng powder manufactured by Office of Monopoly, Republic of Korea and offered by Japan-Korea Korean Ginseng Co., Kobe, at the dose of 2.7 g/day, was performed in patients with hyperlipidemia up to 4 years. The significant increase in serum HDL-cholesterol and also the significant decrease in total cholesterol, atherogenic index, TG, NEFA and lipoperoxide was observed with 3-48 month administration of red ginseng. Conclusions: Red ginseng and ginsenosides improved hyperlipidemia in rats and in man, with the improvement of blood apoproteins, lipoproteins and prostaglandins in experimental hyperlipidemic animals.

• Journal of Mushroom
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• v.19 no.1
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• pp.23-32
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• 2021

This study investigated the anti-hyperlipidemic and anti-obesity effects of Sparassis latifolia (S. latifolia) fruiting body powder in rats fed with a high fat and cholesterol diet (HFD). Rats were fed a normal control diet (ND), an HFD, an HFD supplemented with 5% fruiting body powder of S. latifolia (HFD+SL), or an HFD supplemented with 0.03% simvastatin (HFD+SS), for 6 weeks. The HFD group demonstrated considerable increase in body weight gain, the food efficiency ratio (FER), and plasma cholesterol and triglyceride levels, compared to the ND group. In contrast, the HFD+SL and HFD+SS groups showed significantly reduced body weight gain, food intake, and plasma cholesterol and triglyceride levels compared to the HFD group. In particular, the HFD+SL and HFD+SS diets significantly suppressed the occurrence of non-alcoholic fat deposits in the liver. Taken together, these results suggest that dietary supplementation of the fruiting body powder of S. latifolia in an HFD could lower the risks of hyperlipidemia, atherogenesis, and obesity and may be used as a functional food to manage cardiovascular disease and fecal lipid and cholesterol levels.