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Nam M.-H.,Korean University of Science and Technology | Lee H.-S.,Korea University | Hong C.-O.,Korean University of Science and Technology | Koo Y.-C.,Korean University of Science and Technology | And 2 more authors.
Korean Journal of Food Science and Technology | Year: 2010

Rosa rugosa has traditionally been used as a folk remedy for diabetes. The objective of this study was therefore to demonstrate the inhibition of endothelial dysfunction activities through antioxidants and the anti-glycation of Rosa rugosa roots. Dried roots of Rosa rugosa were boiled in methanol for three hours, evaporated and lyophilized with a freeze-dryer. The methanolic extract of Rosa rugosa roots (RRE) was tested for antioxidant activities by measuring total polyphenol (TP) content, flavonoid content, 1,1-diphenyl-2- picrylhydrazyl free radical-scavenging activity (DPPH) assay, and ferric-reducing antioxidant power (FRAP) assay. The total TP content, flavonoid content, FRAP value, and DPPH-SC50 are 345.2 μg gallic acid equivalents/mg dry matter (DM), 128.1 μg quercetin equivalents/mg DM, 2.2 mM FeSO4/mg DM and 34.2 μg DM/mL, respectively. Treatment of RRE significantly lowered fluorescent formation due to advanced glycation reaction. In addition, reactive oxygen species (ROS) scavenging assay, monocyte adherent assay and transendothelial electrical resistance (TEER) assay were performed to investigate the possibility that RRE improves endothelial dysfunction-induced diabetic complications. The adhesion of THP-1 to treated HUVEC with RRE (100 μg/mL; 33% and 500 μg/mL; 75%) was significantly reduced compared to HUVEC stimulated by glyceraldehydes-AGEs (advanced glycation end product). The TEER value (88 Ω·cm2) of stimulated HUVEC by glyceraldehydes-AGEs was reduced compared to non-stimulation (113 Ω·cm2). However, normalization with RRE increased endothelial permeability in a dose-dependent manner (100 μg/mL; 102 Ω·cm2 and 500 μg/mL; 106 Ω·cm 2). Thus, these results suggest that Rosa rugosa roots could be a novel candidate for the prevention of diabetic complications through antioxidants and inhibition of advanced glycation end product formation. © The Korean Society of Food Science and Technology. Source

Won H.-J.,Korea Institute of Toxicology | Lee H.-S.,Korea University | Kim J.-T.,BioBud Inc. | Hong C.-O.,Korean University of Science and Technology | And 2 more authors.
Korean Journal of Food Science and Technology | Year: 2010

This study was conducted to investigate the anti-diabetic activity of Kocat-D1, which is widely used in traditional medicine to treat diabetes in Shandong, China. Sprague Dawley rats (8 weeks of age) were separated into 4 groups: a normal control, streptozotocin (STZ)-induced diabetic rat group (DM control), Kocat-D1-1 (diabetic rat treated with 0.25 g/kg/day hot water extract), and Kocat-D1-2 (diabetic rat treated with 1 g/kg/day hot water extract). After eight weeks of treatment, the fasting blood glucose levels of the Kocat-D1-1 (334.3±32.9 mg/dL) and Kocat-D1-2 group (259.5±35.0 mg/dL) were significantly lower when compared to the DM control group (451±42.6 mg/dL). Furthermore, the levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), albumin and high-density lipoprotein (HDL) cholesterol in the serum of the Kocat-D1-2 group were significantly normalized when compared to the DM control group. However, significant differences were not observed between the Kocat-D1-1 group and the DM control group. Histochemical staining of the liver of the Kocat-D1-2 group revealed no fat accumulation. The insulin level was significantly upregulated in the Kocat-D1-2 group (0.13±0.02 ng/mL) when compared to the DM control group (0.05±0.04 ng/mL). The relative volume of β-cells in the pancreas of the Kocat-D1-2 group (49.4±4.2%) also increased significantly when compared to the DM control group (12.9±7.9%). These results suggest that Kocat-D1 exerts an anti-hyperglycemic effect through the enhancement of insulin secretion. © The Korean Society of Food Science and Technology. Source

Chung J.H.,Yonsei University | Jeon H.J.,Yonsei University | Hong S.-Y.,Yonsei University | Lee D.L.,BioBud Inc. | And 6 more authors.
PLoS ONE | Year: 2012

Saturated fatty acids are known to activate macrophages and induce vascular inflammation. Although cytokines from activated macrophage influence other vascular cells, the influence of saturated fatty acids on the paracrine effect of macrophages is not fully understood yet. Here we examined the impact of palmitate on the effect of macrophages on vascular smooth muscle cells (SMCs) and their mediators. SMCs proliferation increased significantly after treatment with conditioned media from palmitate-stimulated RAW264.7 cells. SMC migration was found to be greater after treatment with palmitate-conditioned media. SM α-actin and SM22α were decreased in SMCs treated with palmitate-conditioned media. When stimulated with palmitate, RAW264.7 cells secreted more bone morphogenetic protein (BMP)2 and BMP4 into the cell culture media. SMC proliferation, migration, and phenotypic changes were attenuated after treatment of neutralizing antibodies against BMPs or knockdown of BMPs with siRNA. The influences of these proteins were further confirmed by direct treatment of recombinant BMP2 and BMP4 on SMCs. Particularly, the effects of BMPs on SMC migration on phenotypic change were obvious, whereas their effect on SMC proliferation seemed not significant or modest. In conclusion, palmitate promoted macrophages' paracrine effects on SMC proliferation, migration, and phenotypic change. The effect of stimulated macrophages was mediated, at least in part, by BMP2 and BMP4. These results suggest a novel mechanism linking saturated fatty acids and the progression of vascular diseases that is possibly mediated by BMPs from macrophages. © 2012 Chung et al. Source

Nam M.-H.,Korean University of Science and Technology | Lee H.-S.,Korea University | Seomun Y.,BioBud Inc. | Lee Y.,Korean University of Science and Technology | Lee K.-W.,Korean University of Science and Technology
Biochimica et Biophysica Acta - General Subjects | Year: 2011

Background: During hyperglycemia, reducing sugars react with the amino groups to form Amadori products which then form advanced glycation end-products (AGEs). Studies have shown that the AGEs and the receptor binding generated reactive oxygen species, and triggered secretion of cytokines contributing to the local regulations of proliferation and inflammation in cells. Interaction of vessel wall cells and monocytes may trigger the processes leading to atherosclerosis. We evaluated the effects of AGEs on smooth muscle cell (SMC) proliferation and cytokine synthesis in co-cultures of human monocytes (THP-1), endothelial cells (HUVEC) and aortic vascular smooth muscle cell (SMC) to clarify the effects of AGEs on vascular cells and to investigate the mechanisms of arteriosclerosis. Methods: Glycolaldehyde-induced AGEs (glycol-AGEs) was prepared. The THP-1 and HUVEC were cultured with SMC in transwell plates with 100 μg/ml of glycol-AGEs for 24 to 48 h. Results: The proliferation of SMC was induced by glycol-AGEs in the co-culture system. Moreover, SMC treated with glycol-AGEs also expressed interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), and the level of cytokines expression was significantly elevated in the co-culture system of HUVEC and THP-1 when treated with glycol-AGEs. Conclusion: These results suggest that employing a co-culture system is necessary to investigate the synergistic effects of AGEs on intercellular cellular interactions and it creates a more in vivo-like environment for AGEs implicated atherosclerosis research. General significance: All three cell types are required to be investigated together to understand the effects of AGEs on intercellular interactions occurring among these cells. © 2011 Elsevier B.V. All rights reserved. Source

Yang S.-Y.,Korea University | Kang J.H.,Korea University | Seomun Y.,BioBud Inc. | Lee K.-W.,Korea University
Food Science and Biotechnology | Year: 2015

Previously our research found that caffeic acid (CA) has antioxidant activity in vitro and in vivo. However, the antioxidant mechanism of CA has not been clearly demonstrated. We investigated the protective mechanism of CA on oxidative stress in HepG2 cells and primary hepatocytes. We focused on the effects of CA on glutathione (GSH) synthesis and its mechanisms. Reporter gene assay, transient transfection, quantitative reverse transcription-polymerase chain reaction and western blot were performed to confirm the mechanisms of antioxidant capacity. CA increased GSH level and γ-glutamylcysteine ligase (γ-GCL) activity. γ-Glutamylcysteine ligase catalytic subunit (GCLC) mRNA and protein levels were significantly increased following treatment with CA, whereas no changes were observed in the γ-GCL modifier subunit levels in HepG2 and rat hepatocytes. CA phosphorylated JNK, and activated the AP-1 transcription factor. These results show that the intracellular GSH levels and GCLC increased through the JNK/AP-1 pathways by CA treatment. © 2015, The Korean Society of Food Science and Technology and Springer Science+Business Media Dordrecht. Source

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