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Ryowon Choue,Byung Hee Simon Cho 생화학분자생물학회 1997 BMB Reports Vol.30 No.1
The ability of Hep-G2 cells to process [^(125)I]LDL under basal conditions was investigated. The receptor-binding and internalization of [^(125)I]LDL increased with the time of incubation in a saturable manner. After 4 h of incubation, 31.4 ng of [^(125)I]LDL was cell bound. The cells rapidly internalized [^(125)I]LDL via specific, receptor-mediated endocytosis. The amount of internalized [^(125)I]LDL reached a maximun of 96.7 ng at 2 h of incubation and remained constant for the next 2 h. The rate of degradation of internalized [^(125)I]LDL proceeded in a linear manner over the entire 4 h of incubation after an initial lag period. The effects of individial fatty acids (C18:0. C18:1, C18:2. and C18:3), differing in their degree of unsaturation. on the receptor-binding, internalization and degradation of [^(125)I]LDL were also investigated. Inclusion of 1.0 mM of each fatty acid into the culture medium significantly increased [^(125)I]LDL metabolism in Hep-G2 cells. Among the fatty acids tested, stearic acid had the least effect on the receptor-binding activity. There were no significant differences among the unsaturated fatty acids in LDL-receptor binding. The effect of individual fatty acids on the [^(125)I]LDL uptake was similar to that of the receptor-binding. showing a significantly lower effect with stearic acid. The amount of degraded material of internalized [^(125)I]LDL was the lowest with stearic acid when it was compared with unsaturated fatty acids.
Yim, Jungeun,Choue, Ryowon,Park, Changshin,Cha, Youngnam,Chyun, Jonghee The Korean Nutrition Society 2004 Nutritional Sciences Vol.7 No.4
Dietary intervention and simvastatin is beneficial in the prevention cardiovascular diseases by lowering plasma lipid levels. Endothelial dysfunction is associated with coronary artery disease and its risk factors and is reversed by dietary intervention. It has been suggested that hyperlipidemia contributes to the development of atherosclerosis by increasing inducible nitric oxide synthase (iNOS) expression via intimal thickening. Statins treatment has been found to decrease iNOS expression and atherogenensis in animal models. We hypothesized that dietary intervention and simvastatin therapy could decrease plasma nitric oxide in hypercholesterolemic patients, which would suggest the opportunity for modulation of iNOS expression through the use of statins in a clinical situation. We measured the plasma levels of nitrite and nitrate (NOx) in 19 hyperlipidemia patients. The subjects were under dietary intervention following simvastatin therapy for 12 weeks. As a result, the plasma level of NOx, stable metabolites of nitric oxide (NO), saw a two-fold elevation in hyperlipidemic patients as compared to normal levels. Although 12 weeks of dietary intervention did not lower NOx levels, subsequent 12-week simvastatin (10 mg/day) treatment, along with dietary intervention, lowered NOx levels significantly. This NOx reduction, induced by simvastatin therapy, positively correlated with lowered coronary risk factors (r=0.40, p=0.02). It indicated that simvastatin therapy decreases plasma NOx levels by, perhaps, decreasing iNOS expression or activity leading to the attenuation of the development of neointima.