• 동의생리병리학회지
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• 제23권5호
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• pp.1019-1024
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• 2009

Diabetic neuropathy is characterized by the decrease of cell viability in neuron, which is induced by the hyperglycemia. HT22 cell is the neuron cell line originated from hippocampus. Ginsenosides have been reported to retain anti-diabetic effect. However, the preventive effect of ginsenosides in the condition of diabetic neuropathy was not elucidated. Thus, this study was conducted to examine the protective effect of ginsenoside total saponin (GTS), panoxadiol (PD), and panoxatriol (PT) in the high glucose-induced cell death of HT22 cells, an in vitro cellular model for diabetic neuropathy. In present study, high glucose increased lactate dehydrogenase(LDH) activity, the lipid peroxide(LPO) formation and induced the decrease of cell viability. These effects were completely prevented by the treatment of GTS, but partially prevented by the treatment of PD and PT. High glucose also increased the expression of Bax and cleaved form of caspase-3 but decreased that of Bcl-2. These effects of high glucose on Bax, Bcl-2 and cleaved form of caspase-3 were completely prevented by the treatment of GTS, but partially prevented by the treatment of PD and PT in HT22 cells. In conclusion, ginsenosides prevented high glucose-induced cell death of hippocampal neuron through the inhibition of oxidative stress and apoptosis in HT 22 cells.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
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• pp.80-80
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• 2003

Insulin-dependent or Type 1 diabetes mellitus (IDDM) has been associated with an increased severity of periodontal disease. Since periodontal ligament (PDL) cells play a significant role in maintenance and regeneration of mineralized tissue, the success of procedures, such as guided tissue regeneration, is directly related to the ability of these cells to augment mineralized tissue. In this study, we investigated the time- and dose-dependent effect of high glucose on the proliferation and collagen synthesis of human periodontal ligament (PDL) cells. PDL cells were treated with high glucose (22mM, 33mM, 44mM) for 1 or 2 days. High glucose significantly inhibited proliferation of PDL cells as a time- and dose-dependent manner as evidenced by MTT assay. PDL cells were cultured in high glucose media (22mM, 33mM, 44mM) for 24 h. The ratio of collagen content to total protein was evaluated, and the gene expression of type I collagen was assessed by RT - PCR. The high concentration of glucose inhibited collagen synthesis, a marker of bone formation activity. This study indicated high glucose concentration could alter the metabolism of periodontal ligament cell, leading to alveolar bone destruction.

• Preventive Nutrition and Food Science
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• 제19권3호
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• pp.170-177
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• 2014

Endothelial cell dysfunction is considered to be a major cause of vascular complications in diabetes. In the present study, we investigated the protective effect of a baechu kimchi added Ecklonia cava extract (BKE) against high glucose induced oxidative damage in human umbilical vein endothelial cells (HUVECs). Treatment with a high concentration of glucose (30 mM) induced cytotoxicity, whereas treatment with BKE protected HUVECs from high glucose induced damage; by restoring cell viability. In addition, BKE reduced lipid peroxidation, intracellular reactive oxygen species and nitric oxide levels in a dose dependent manner. Treatment with high glucose concentrations also induced the overexpression of inducible nitric oxide synthase, cyclooxygenase-2 and NF-${\kappa}B$ proteins in HUVECs, but BKE treatment significantly reduced the overexpression of these proteins. These findings indicate that BKE may be a valuable treatment against high glucose-induced oxidative stress HUVECs.

• Preventive Nutrition and Food Science
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• 제11권2호
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• pp.94-99
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• 2006

This study investigated the protective effect of the butanol (BuOH) fraction from Laminaria japonica (BFLJ) extract on high glucose-induced oxidative stress in human umbilical vein endothelial cells (HUVECs). Freeze-dried L japonica was extracted with distilled water, and the extracted solution was mixed with ethanol then centrifuged. The supernatant was subjected to sequential fractionation with various solvents. The BuOH fraction was used in this study because it possessed the strongest antioxidant activity among the various solvent fractions. To determine the protective effect of the BFLJ, oxidative stress was induced by exposing of HUVECs to the high glucose (30 mM) or normal glucose (5.5 mM) for 48 hr. Cell viability, lipid peroxidation, glutathione (GSH) concentration, and antioxidant enzyme activities such as catalase, superoxide dismutase (SOD), glutathione peroxidase (GSH-px), and glutathion reductase (GSH-re) were measured. Exposure of HUVECs to high glucose for 48 hr resulted in a significant (p<0.05) decrease in cell viability, SOD, GSH-px and GSH-re and a significant (p<0.05) increase in thiobarbituric acid reactive substances (TBARS) formation in comparison to the cells treated with 5.5 mM glucose or untreated with glucose. BFLJ treatment decreased TBARS formation and increased cell viability, GSH concentration, and activities of antioxidant enzymes including catalase, SOD, GSH-px, and GSH-re in high glucose pretreated HUVECs. These results suggest that BFLJ may be able to protect HUVECs from high glucose-induced oxidative stress, partially through the antioxidative defence systems.

• Nutritional Sciences
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• 제9권1호
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• pp.3-8
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• 2006

Functional damage to microvascular endothelial cells by hyperglycemia is thought to be one of the critical risk factor.; in the impaired wound healing seen with diabetes mellitus. It is also thought that oxidative stress plays a significant role in this endothelial cell dysfunction. The present study examined the differential effects of flavonoids on endothelial cell dysfunction under high glucose conditions. Human endothelial cells exposed to 30 mmol/L glucose for 7 d were pre-treated with various flavonoids and pulse-treated with 0.2 mmol/L $H_2O_2$ for 30 min. High glucose markedly decreased cell viability with elevated oxidant generation and nuclear condensation. $H_2O_2$ insult exacerbated endothelial cytotoxicity due to chronic exposure to high glucose. (-)Epigallocatechin gallate and quercetin improved glucose-induced cell damage with the disappearnnce of apoptotic bodies, whereas apigenin intensified the glucose cytotoxicity. In addition, cell viability data revealed that these flavonoids of (-)epigallocatechin gallate and quercetin substantially attenuated both high glucose- and $H_2O_2$- induced dual endothelial damage. These results suggest that (-)epigallocatechin gallate and quercetin may be beneficial agents for improving endothelial cell dysfunction induced by high glucose and may prevent or reduce the development of diabetic vascular complications.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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• pp.147-147
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• 2002

In this study, a mechanism by which glucose level modulates glucose transport in Jurkat cells was investigated. Glucose uptake was more efficient in the cells cultivated in low glucose (2.5 mM) medium than that grown in high glucose (20 $\mu$M) medium. Vmax (0.74 n㏖/10$^6$ cells$\cdot$min) of glucose uptake measured with the cells grown in the low glucose medium was higher than the one (1.06 n㏖/10$^6$ cells$\cdot$min) in the high glucose medium while Km was almost consistent through the change of glucose levels, indicating the increase of glucose transporter number.

• Nutrition Research and Practice
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• 제8권5호
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• pp.494-500
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• 2014

BACKGROUND/OBJECTIVES: This study investigated whether Padina arborescens extract (PAE) protects INS-1 pancreatic ${\beta}$ cells against glucotoxicity-induced apoptosis. MATERIALS/METHODS: Assays, including cell viability, lipid peroxidation, generation of intracellular ROS, NO production, antioxidant enzyme activity and insulin secretion, were conducted. The expressions of Bax, Bcl-2, and caspase-3 proteins in INS-1 cells were evaluated by western blot analysis, and apoptosis/necrosis induced by high glucose was determined by analysis of FITC-Annexin V/PI staining. RESULTS: Treatment with high concentrations of glucose induced INS-1 cell death, but PAE at concentrations of 25, 50 or $100{\mu}g/ml$ significantly increased cell viability. The treatment with PAE dose dependently reduced the lipid peroxidation and increased the activities of antioxidant enzymes reduced by 30 mM glucose, while intracellular ROS levels increased under conditions of 30 mM glucose. PAE treatment improved the secretory responsiveness following stimulation with glucose. The results also demonstrated that glucotoxicity-induced apoptosis is associated with modulation of the Bax/Bcl-2 ratio. When INS-1 cells were stained with Annexin V/PI, we found that PAE reduced apoptosis by glucotoxicity. CONCLUSIONS: In conclusion, the present study indicates that PAE protects against high glucose-induced apoptosis in pancreatic ${\beta}$ cells by reducing oxidative stress.

• The Korean Journal of Physiology and Pharmacology
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• 제9권4호
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• pp.195-201
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• 2005

High extracellular glucose concentration was reported to suppress intracellular $Ca^{2+}$ clearing through altered sarcoplasmic reticulum (SR) function. In the present study, we attempted to elucidate the effects of pyruvate and fatty acid on SR function and reveal the mechanistic link with glucose-induced SR dysfunction. For this purpose, SR $Ca^{2+}$-uptake rate was measured in digitonin-permeabilized H9c2 cardiomyocytes cultured in various conditions. Exposure of these cells to 5 mM pyruvate for 2 days induced a significant suppression of SR $Ca^{2+}$-uptake, which was comparable to the effects of high glucose. These effects were accompanied with decreased glucose utilization. However, pyruvate could not further suppress SR $Ca^{2+}$-uptake in cells cultured in high glucose condition. Enhanced entry of pyruvate into mitochondria by dichloroacetate, an activator of pyruvate dehydrogenase complex, also induced suppression of SR $Ca^{2+}$-uptake, indicating that mitochondrial uptake of pyruvate is required in the SR dysfunction induced by pyruvate or glucose. On the other hand, augmentation of fatty acid supply by adding 0.2 to 0.8 mM oleic acid resulted in a dose-dependent suppression of SR $Ca^{2+}$-uptake. However, these effects were attenuated in high glucose-cultured cells, with no significant changes by oleic acid concentrations lower than 0.4 mM. These results demonstrate that (1) increased pyruvate oxidation is the key mechanism in the SR dysfunction observed in high glucose-cultured cardiomyocytes; (2) exogenous fatty acid also suppresses SR $Ca^{2+}$-uptake, presumably through a mechanism shared by glucose.

• Fisheries and Aquatic Sciences
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• 제23권9호
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• pp.24.1-24.9
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• 2020

Brown alga (Ishige okamurae; IO) dietary supplements have been reported to possess anti-diabetic properties. However, the effects of IO supplements have not been evaluated on glucose metabolism in the pancreas and skeletal muscle. C57BL/6 N male mice (age, 7 weeks) were arranged in five groups: a chow diet with 0.9% saline (NFD/saline group), high-fat diet (HFD) with 0.9% saline (HFD/saline group). high-fat diet with 25 mg/kg IO extract (HFD/25/IOE). high-fat diet with 50 mg/kg IO extract (HFD/50/IOE), and high-fat diet with 75 mg/kg IO extract (HFD/75/IOE). After 4 weeks, the plasma, pancreas, and skeletal muscle samples were collected for biochemical analyses. IOE significantly ameliorated glucose tolerance impairment and fasting and 2 h blood glucose level in HFD mice. IOE also stimulated the protein expressions of the glucose transporters (GLUTs) including GLUT2 and GLUT4 and those of their related transcription factors in the pancreases and skeletal muscles of HFD mice, enhanced glucose metabolism, and regulated blood glucose level. Our results suggest Ishige okamurae extract may reduce blood glucose levels by improving glucose metabolism in the pancreas and skeletal muscle in HFD-induced diabetes.

• Preventive Nutrition and Food Science
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• 제10권1호
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• pp.52-57
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• 2005

Soy and soy foods are a rich source of isoflavones, which possess several biological activities. The effect of soy isoflavones, genistin and diadzin and their respective aglycones, on glucose uptake in adipocytes isolated from normal or high-fat fed rats was examined. As expected, insulin stimulated glucose uptake in a concentration-dependent manner. However, genistin and daidzin and their aglycones inhibited glucose uptake in a concentration-dependent (25-100μM) manner. In a time-course response, the aglycones significantly inhibited glucose uptake throughout 3 hr (after 30, 60, 120, 180 min), whereas the glycones only significantly inhibited the glucose uptake after 120 min and 180 min in the isolated rat adipocytes. Thus, the glucosides of genistein and daidzein, i.e. genistin and daidzin, were much less effective in inhibiting glucose uptake than their aglycones. In addition, genistin and daidzin did not significantly affect the insulin-stimulated glucose uptake, whereas genistein and daidzein did significantly inhibited glucose uptake compared to the vehicle control group by 47.5% and 24.8%, respectively (p < 0.05). The isoflavones also significantly inhibited glucose uptake in adipocytes isolated from rats fed a high-fat diet (50% of total calorie intake) when compared to the vehicle control. Finally, the isoflavones were found to enhance lipolysis in adipocytes isolated from high-fat fed rats, where the glycerol released by the aglycones was also higher than that released by the glycones. The current results showed that the inhibitory effect of daidzein on glucose uptake was very similar to that of genistein. The aglycones were more potent in inhibiting the uptake of glucose and a more potent stimulator of lypolysis than the glycones in adipocytes isolated from high-fat fed rats.