• 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 the Korean Society of Food Science and Nutrition
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• v.23 no.3
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• pp.530-539
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• 1994

All lipoproteins are made up of three major classes of lipids : triglycerides, cholesterol, and phospholipids. Lipoproteins vary in their relative content of these lipids as well as in size and protein content. Human low density lipoprotein (LDL) is a main carrier for cholesterol in the blood stream, and it is well established that cholesterol deposits in the arteries stem primarily from LDL and that increased levels of plasma LDL correlated with in increased risk of atherosclerosis. Various lines of research provide strong evidence that lDL may become oxidized in vivo and that oxidized-LDL is the species involved in the formation of early atherosclerotic lesions. the most crucial findings in this context are the following : (1) Oxidized -LDL has chemotactic properties and if present in the intimal space of the arteries would recruit blood monocytes which then can develop into tissue macrophages ; (2) marcrophages take up oxidized-LDL unregulated to from lipid laden foam cells ; (3) Oxdized-LDLis highly cytotoxic and could be responsible for damage of the endothelial layer and for the destruction of smooth muscle cells.

• Korean Journal of Food Science and Technology
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• v.36 no.2
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• pp.311-316
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• 2004

Antioxidant effects of Rosa davurica Pall extract on copper-mediated LDL oxidative modification were investigated. Oxidation products of LDL were determined based on TBA value, formation of conjugate diene, and apolipoprotein carbonyl value. As revealed through TBA values, ethyl acetate and butanol fractions of R. davurica Pall root showed strong antioxidant effect, with 85.3 and 93.2% inhibitions at $30\;{\mu}g/mL$ each, respectively. Ethyl acetate and butanol fractions at $30\;{\mu}g/mL$ inhibited LDL oxidation up to 8 hr. Conjugate diene formation by lipid oxidation with $Cu^{2+}$ addition in ethyl acetate and butanol fractions decreased 2.2-and 5.6-fold, respectively, compared to control. Carbonyl value decreased in the presence of butanol and ethyl acetate fractions. Methanol and ethyl acetate extracts of R. davurica Pall root showed higher absorbancy at 285 nm. Ethanol extract of R. davurica Pall root and stem contained 10.6 g/100 g total phenolic compounds. Results reveal phenolic compound as major biological component in R. davurica Pall extracts. Ethyl acetate and butanol fraction showed strongest antioxidant effect on LDL oxidation.

• Proceedings of the Korea Society of Poultry Science Conference
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• 2003.11a
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• pp.9-27
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• 2003

This study was performed to measure the effect of carotenoid polarity on absorption and Pigmentation in blood, muscle, and skin of laying hens. Carotenoids used in this study and Polarity were ${\beta}$-8-Apo-carotenoic acid ethyl ester(ACAEE) ＞ astaxanthin ＞ canthaxanthin ＞ ${\beta}$-carotene. The chickens used in this study were 61∼78 weeks old ISA brown laying hens. Experiment #1 was designed to measure the effect of carotenoid level on the accumulation of carotenoids in carcass of laying hens after feeding for 6 weeks. D-carotene was accumulated in skin only at a detectable level when it was fed at 300 mg/kg feed. The skin was pigmented as yellow when it was measured by colorimeter. The concentration of ${\beta}$-carotene in blood was proportional to that in the feed. Pigmentation of muscle by 9-carotene was not effective. Canthaxanthin significantly increased redness of the skin(p＜0.05). However, canthaxanthin did not pigment muscle. The level of canthaxanthin in the blood and skin increased as the concentration in feed increased. ACAEE at 200 and 300 mg/kg feed significantly increased yellowness of the skin(p＜0.05). At all levels of ACAEE used($\geq$50 mg/kg feed) the b values of colorimeter increased. With increases in the contents of ACAEE, the concentration of ACAEE in the blood and skin increased. Compared to ${\beta}$-carotene, ACAEE and canthaxanthin were absorbed 9- and 3-fold more into the blood, respectively. The concentration of ACAEE and canthaxanthin in the skin was 1/10 of those in the blood. The lower were the concentrations of carotenoids in the feed, the higher were the absorption rates(from feed to blood and from blood to skin) The results indicated that the higher was the polarity of carotenoids, the more effective were the absorption and pigmentation. In experiment #2, the effect of carotenoid levels of feed on the accumulation of carotenoids in each body part of laying hens was determined. The colorimeter values for redness and yellowness significantly increased when canthaxanthin was fed at $\geq$50 mg/kg feed(p＜0.05). Breast and thigh were not affected by feeding of canthaxanthin at the levels used. The L values of muscle but not the a and b values were significantly affected by feeding at $\geq$200 mg/kg feed for wings and breasts, respectively. The yellowness of skin and muscle significantly increased when ACAEE was fed at $\geq$ 100 and $\geq$ 200 mg/kg feed, respectively(p＜0.05).

• BMB Reports
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• v.53 no.2
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• pp.100-105
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• 2020

While liver histopathology is heterogeneous in diabetes, the underlying mechanisms remain unclear. We investigated whether glycemic variation resulting from differential diets can induce heterogeneity in diabetic liver and the underlying molecular mechanisms. We generated end-stage non-obese diabetic model rats by subtotal-pancreatectomy in male Sprague-Dawley rats and ad libitum diet for 7 weeks (n = 33). The rats were then divided into three groups, and fed a standard- or a low-protein diet (18 or 6 kcal%, respectively), for another 7 weeks: to maintain hyperglycemia, 11 rats were fed ad libitum (18AL group); to achieve euglycemia, 11 were calorie-restricted (18R group), and 11 were both calorie- and protein-restricted with the low-protein diet (6R group). Overnight-fasted liver samples were collected after the differential diets together with sham-control (18S group), and histology and molecular changes were compared. Hyperglycemic-18AL showed glycogenic hepatopathy (GH) without steatosis, with the highest GSK-3β inactivation because of Akt activation during hyperglycemia; mitochondrial function was not impaired, compared to the 18S group. Euglycemic-18R showed neither GH nor steatosis, with intermediate GSK-3β activation and mitochondrial dysfunction. However, euglycemic-6R showed both GH and steatosis despite the highest GSK-3β activity and no molecular evidence of increased lipogenesis or decreased ApoB expression, where mitochondrial dysfunction was highest among the groups. In conclusion, heterogeneous liver histopathology developed in end-stage non-obese diabetic rats as the glycemic levels varied with differential diets, in which protein content in the diets as well as glycemic levels differentially influenced GSK-3β activity and mitochondrial function in insulin-deficient state.