• Investigative Magnetic Resonance Imaging
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• v.13 no.1
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• pp.81-87
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• 2009

Purpose : We sought to evaluate enhancement of plaque with gadolinium-based contrast agent by magnetic resonance imaging (MRI) in comparison with histopathology, namely lipid-rich and macrophage-rich components that were two representative characteristics of plaque vulnerability using atherosclerotic rabbit aorta in order to determine which histopathologic component is relevant to the enhancement. Materials and Methods : New Zealand white rabbit (n=4, weight 3.0 to 3.5 kg, all male) was used for animal model of atherosclerosis. Atherosclerotic aortic lesions were induced by high-cholesterol diet and double balloon injury. T1-weight axial images were acquired before and after gadolinium-based contrast agent using a 3-T MRI. MR images and the matched histopathological sections (n=35) were divided into 4 quadrants or 3 (n=130). Enhancement ratio (ER, ER=SIpost/SIpre) on MRI was calculated for each quadrant and compared with histopathology in regard to lipid-rich and macrophage-rich areas. Results : Lipid-rich quadrants were 72 and fibrous quadrants were 58. The number of quadrants which had macrophage-rich areas was 105 and that of quadrants which did not have macrophage-rich areas was 25. ER was significantly higher in lipid-rich quadrants than in fibrous quadrants (mean ER 2.25c$\pm$0.41 vs. 2.72$\pm$0.65, p=0.013). ER poorly correlated with macrophage-rich areas when lipid-component was controlled (correlation coefficient -0.203, p=0.236). Conclusion : Lipid-rich plaques showed stronger enhancement than fibrous plaques using a standard gadolinium-based extracellular contrast agent. Macrophage infiltration did not correlate with degree of enhancement. Further study is warranted that account for optimal time of imaging after contrast injection using various plaque models from early to advanced stages and all possible parameters associated with contrast enhancement.

• Journal of Ginseng Research
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• v.41 no.3
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• pp.257-267
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• 2017

Background: Heat-processed ginseng, sun ginseng (SG), has been reported to have improved therapeutic properties compared with raw forms, such as increased antidiabetic, anti-inflammatory, and antihyperglycemic effects. The aim of this study was to investigate the antiobesity effects of SG through the suppression of cell differentiation and proliferation of mouse 3T3-L1 preadipocyte cells and the lipid accumulation in Caenorhabditis elegans. Methods: To investigate the effect of SG on adipocyte differentiation, levels of stained intracellular lipid droplets were quantified by measuring the oil red O signal in the lipid extracts of cells on differentiation Day 7. To study the effect of SG on fat accumulation in C. elegans, L4 stage worms were cultured on an Escherichia coli OP50 diet supplemented with $10{\mu}g/mL$ of SG, followed by Nile red staining. To determine the effect of SG on gene expression of lipid and glucose metabolism-regulation molecules, messenger RNA (mRNA) levels of genes were analyzed by real-time reverse transcription-polymerase chain reaction analysis. In addition, the phosphorylation of Akt was examined by Western blotting. Results: SG suppressed the differentiation of 3T3-L1 cells stimulated by a mixture of 3-isobutyl-1-methylxanthine, dexamethasone, and insulin (MDI), and inhibited the proliferation of adipocytes during differentiation. Treatment of C. elegans with SG showed reductions in lipid accumulation by Nile red staining, thus directly demonstrating an antiobesity effect for SG. Furthermore, SG treatment down-regulated mRNA and protein expression levels of peroxisome proliferator-activated receptor subtype ${\gamma}$ ($PPAR{\gamma}$) and CCAAT/enhancer-binding protein-alpha ($C/EBP{\alpha}$) and decreased the mRNA level of sterol regulatory element-binding protein 1c in MDI-treated adipocytes in a dose-dependent manner. In differentiated 3T3-L1 cells, mRNA expression levels of lipid metabolism-regulating factors, such as amplifying mouse fatty acid-binding protein 2, leptin, lipoprotein lipase, fatty acid transporter protein 1, fatty acid synthase, and 3-hydroxy-3-methylglutaryl coenzyme A reductase, were increased, whereas that of the lipolytic enzyme carnitine palmitoyltransferase-1 was decreased. Our data demonstrate that SG inversely regulated the expression of these genes in differentiated adipocytes. SG induced increases in the mRNA expression of glycolytic enzymes such as glucokinase and pyruvate kinase, and a decrease in the mRNA level of the glycogenic enzyme phosphoenol pyruvate carboxylase. In addition, mRNA levels of the glucose transporters GLUT1, GLUT4, and insulin receptor substrate-1 were elevated by MDI stimulation, whereas SG dose-dependently inhibited the expression of these genes in differentiated adipocytes. SG also inhibited the phosphorylation of Akt (Ser473) at an early phase of MDI stimulation. Intracellular nitric oxide (NO) production and endothelial nitric oxide synthase mRNA levels were markedly decreased by MDI stimulation and recovered by SG treatment of adipocytes. Conclusion: Our results suggest that SG effectively inhibits adipocyte proliferation and differentiation through the downregulation of $PPAR{\gamma}$ and $C/EBP{\alpha}$, by suppressing Akt (Ser473) phosphorylation and enhancing NO production. These results provide strong evidence to support the development of SG for antiobesity treatment.

• Journal of Life Science
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• v.24 no.6
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• pp.686-693
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• 2014

Restricted supply of nutrients may affect genes at the molecular level as well as physiological functions. Understanding the cellular responses during starvation is necessary for developing strategies to reduce damage caused by starvation stress. After 1 h of starvation, Got1 gene expression was increased but its expression returned to the normal state after 24 h. Mat1 gene expression continuously increased with starvation from 1 h until 24 hr. Rats starved for 1-3 days showed significant changes in expression of the Got1 and Mat1 genes, which were significantly reduced in the cerebral cortex and cerebellum. In the lung, gene expression was increased by starvation for 1-2 days but decreased on the third day. No differences were observed in gene expression in the heart. Strong Got1 lung gene expression was seen in the starvation group one day after restoration of the food supply. Muscle mass was significantly reduced at the start of starvation and remained the same after two days of starvation and one day after the food supply was restored. The Mat1 gene expression did not change. The Got1 was induced by NaCl and showed strong expression in the lung and the thymus, but the apparent decrease of the remaining changes were not observed in male rats. The Mat1 gene was not as sensitive as the Got1 gene to induction by NaCl. However, differences in gene induction by NaCl were evident between males and females, indicating that diet control of gene expression is associated with hormones.