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Repeated Glucose Deprivation/Reperfusion Induced PC-12 Cell Death through the Involvement of FOXO Transcription Factor
Na Han, You Jeong Kim, Su Min Park, Seung Man Kim, Ji Suk Lee, Hye Sook Jung, Eun Ju Lee, Tae Kyoon Kim, Tae Nyun Kim, Min Jeong Kwon, Soon Hee Lee, Mi-kyung Kim, Byoung Doo Rhee, Jeong Hyun Park
Diabetes Metab J. 2016;40(5):396-405.   Published online September 1, 2016
DOI: https://doi.org/10.4093/dmj.2016.40.5.396
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  • 1 Crossref
AbstractAbstract PDFPubReader   
Background

Cognitive impairment and brain damage in diabetes is suggested to be associated with hypoglycemia. The mechanisms of hypoglycemia-induced neural death and apoptosis are not clear and reperfusion injury may be involved. Recent studies show that glucose deprivation/reperfusion induced more neuronal cell death than glucose deprivation itself. The forkhead box O (FOXO) transcription factors are implicated in the regulation of cell apoptosis and survival, but their role in neuronal cells remains unclear. We examined the role of FOXO transcription factors and the involvement of the phosphatidylinositol 3-kinase (PI3K)/Akt and apoptosis-related signaling pathways in PC-12 cells exposed to repeated glucose deprivation/reperfusion.

Methods

PC-12 cells were exposed to control (Dulbecco's Modified Eagle Medium [DMEM] containing 25 mM glucose) or glucose deprivation/reperfusion (DMEM with 0 mM glucose for 6 hours and then DMEM with 25 mM glucose for 18 hours) for 5 days. MTT assay and Western blot analysis were performed for cell viability, apoptosis, and the expression of survival signaling pathways. FOXO3/4',6-diamidino-2-phenylindole staining was done to ascertain the involvement of FOXO transcription factors in glucose deprivation/reperfusion conditions.

Results

Compared to PC-12 cells not exposed to hypoglycemia, cells exposed to glucose deprivation/reperfusion showed a reduction of cell viability, decreased expression of phosphorylated Akt and Bcl-2, and an increase of cleaved caspase-3 expression. Of note, FOXO3 protein was localized in the nuclei of glucose deprivation/reperfusion cells but not in the control cells.

Conclusion

Repeated glucose deprivation/reperfusion caused the neuronal cell death. Activated FOXO3 via the PI3K/Akt pathway in repeated glucose deprivation/reperfusion was involved in genes related to apoptosis.

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  • Predictive factors for the development of diabetes in cancer patients treated with phosphatidylinositol 3-kinase inhibitors
    Gyuri Kim, Myungeun Yoo, Min Hee Hong, Byung-Wan Lee, Eun Seok Kang, Bong-Soo Cha, Hye Ryun Kim, Yong-ho Lee, Byoung Chul Cho
    Cancer Chemotherapy and Pharmacology.2019; 84(2): 405.     CrossRef
Current Status of Prescription in Type 2 Diabetic Patients from General Hospitals in Busan
Ji Hye Suk, Chang Won Lee, Sung Pyo Son, Min Cheol Kim, Jun Hyeob Ahn, Kwang Jae Lee, Ja Young Park, Sun Hye Shin, Min Jeong Kwon, Sang Soo Kim, Bo Hyun Kim, Soon Hee Lee, Jeong Hyun Park, In Joo Kim
Diabetes Metab J. 2014;38(3):230-239.   Published online June 17, 2014
DOI: https://doi.org/10.4093/dmj.2014.38.3.230
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  • 9 Web of Science
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AbstractAbstract PDFPubReader   
Background

Data regarding the prescription status of individuals with diabetes are limited. This study was an analysis of participants from the relationship between cardiovascular disease and brachial-ankle pulse wave velocity in patients with type 2 diabetes (REBOUND) Study, which was a prospective multicenter cohort study recruited from eight general hospitals in Busan, Korea. We performed this study to investigate the current status of prescription in Korean type 2 diabetic patients.

Methods

Type 2 diabetic patients aged 30 years or more were recruited and data were collected for demographics, medical history, medications, blood pressure, and laboratory tests.

Results

Three thousands and fifty-eight type 2 diabetic patients were recruited. Mean age, duration of diabetes, and HbA1c were 59 years, 7.6 years, and 7.2%, respectively. Prevalence of hypertension was 66%. Overall, 7.3% of patients were treated with diet and exercise only, 68.2% with oral hypoglycemic agents (OHAs) only, 5.3% with insulin only, and 19.2% with both insulin and OHA. The percentage of patients using antihypertensive, antidyslipidemic, antiplatelet agents was similar as about 60%. The prevalence of statins and aspirin users was 52% and 32%, respectively.

Conclusion

In our study, two thirds of type 2 diabetic patients were treated with OHA only, and one fifth with insulin plus OHA, and 5% with insulin only. More than half of the patients were using each of antihypertensive, antidyslipidemic, or antiplatelet agents. About a half of the patients were treated with statins and one third were treated with aspirin.

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  • A double‐blind, Randomized controlled trial on glucose‐lowering EFfects and safety of adding 0.25 or 0.5 mg lobeglitazone in type 2 diabetes patients with INadequate control on metformin and dipeptidyl peptidase‐4 inhibitor therapy: REFIND study
    Soree Ryang, Sang Soo Kim, Ji Cheol Bae, Ji Min Han, Su Kyoung Kwon, Young Il Kim, Il Seong Nam‐Goong, Eun Sook Kim, Mi‐kyung Kim, Chang Won Lee, Soyeon Yoo, Gwanpyo Koh, Min Jeong Kwon, Jeong Hyun Park, In Joo Kim
    Diabetes, Obesity and Metabolism.2022; 24(9): 1800.     CrossRef
  • Arterial stiffness is an independent predictor for risk of mortality in patients with type 2 diabetes mellitus: the REBOUND study
    Jeong Mi Kim, Sang Soo Kim, In Joo Kim, Jong Ho Kim, Bo Hyun Kim, Mi Kyung Kim, Soon Hee Lee, Chang Won Lee, Min Chul Kim, Jun Hyeob Ahn, Jinmi Kim
    Cardiovascular Diabetology.2020;[Epub]     CrossRef
  • Efficacy and Safety of Pioglitazone versus Glimepiride after Metformin and Alogliptin Combination Therapy: A Randomized, Open-Label, Multicenter, Parallel-Controlled Study
    Jeong Mi Kim, Sang Soo Kim, Jong Ho Kim, Mi Kyung Kim, Tae Nyun Kim, Soon Hee Lee, Chang Won Lee, Ja Young Park, Eun Sook Kim, Kwang Jae Lee, Young Sik Choi, Duk Kyu Kim, In Joo Kim
    Diabetes & Metabolism Journal.2020; 44(1): 67.     CrossRef
  • Efficacy and safety of sitagliptin/metformin fixed‐dose combination compared with glimepiride in patients with type 2 diabetes: A multicenter randomized double‐blind study
    Sang Soo Kim, In Joo Kim, Kwang Jae Lee, Jeong Hyun Park, Young Il Kim, Young Sil Lee, Sung Chang Chung, Sang Jin Lee
    Journal of Diabetes.2017; 9(4): 412.     CrossRef
  • Arterial Stiffness Is More Associated with Albuminuria than Decreased Glomerular Filtration Rate in Patients with Type 2 Diabetes Mellitus: The REBOUND Study
    Jong Ho Kim, Sang Soo Kim, In Joo Kim, Bo Hyun Kim, Ja Young Park, Chang Won Lee, Ji Hye Suk, Sun Hae Shin, Sung Pyo Son, Min Chul Kim, Jun Hyeob Ahn, Kwang Jae Lee, Min Jung Kwon, Soon Hee Lee, Jeong Hyun Park
    Journal of Diabetes Research.2017; 2017: 1.     CrossRef
  • Insulin therapy for adult patients with type 2 diabetes mellitus: a position statement of the Korean Diabetes Association, 2017
    Byung-Wan Lee, Jin Hwa Kim, Seung-Hyun Ko, Kyu Yeon Hur, Nan-Hee Kim, Sang Youl Rhee, Hyun Jin Kim, Min Kyong Moon, Seok-O Park, Kyung Mook Choi
    The Korean Journal of Internal Medicine.2017; 32(6): 967.     CrossRef
  • Insulin Therapy for Adult Patients with Type 2 Diabetes Mellitus: A Position Statement of the Korean Diabetes Association, 2017
    Byung-Wan Lee, Jin Hwa Kim, Seung-Hyun Ko, Kyu-Yeon Hur, Nan-Hee Kim, Sang Youl Rhee, Hyun Jin Kim, Min Kyong Moon, Seok-O Park, Kyung Mook Choi
    Diabetes & Metabolism Journal.2017; 41(5): 367.     CrossRef
  • Reduction of Sulfonylurea with the Initiation of Basal Insulin in Patients with Inadequately Controlled Type 2 Diabetes Mellitus Undergoing Long-Term Sulfonylurea-Based Treatment
    Yeoree Yang, Jeong-Ah Shin, Hae Kyung Yang, Seung-Hwan Lee, Seung-Hyun Ko, Yu-Bae Ahn, Kun-Ho Yoon, Jae-Hyoung Cho
    Diabetes & Metabolism Journal.2016; 40(6): 454.     CrossRef
  • Comparison of Vildagliptin and Pioglitazone in Korean Patients with Type 2 Diabetes Inadequately Controlled with Metformin
    Jong Ho Kim, Sang Soo Kim, Hong Sun Baek, In Kyu Lee, Dong Jin Chung, Ho Sang Sohn, Hak Yeon Bae, Mi Kyung Kim, Jeong Hyun Park, Young Sik Choi, Young Il Kim, Jong Ryeal Hahm, Chang Won Lee, Sung Rae Jo, Mi Kyung Park, Kwang Jae Lee, In Joo Kim
    Diabetes & Metabolism Journal.2016; 40(3): 230.     CrossRef
The Effects of Glyburide on Apoptosis and Endoplasmic Reticulum Stress in INS-1 Cells in a Glucolipotoxic Condition
Min Jeong Kwon, Hye Suk Chung, Chang Shin Yoon, Jung Hae Ko, Hae Jung Jun, Tae Kyun Kim, Soon Hee Lee, Kyung Soo Ko, Byoung Doo Rhee, Mi Kyung Kim, Jeong Hyun Park
Diabetes Metab J. 2011;35(5):480-488.   Published online October 31, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.5.480
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AbstractAbstract PDFPubReader   
Background

β-cell death due to endoplasmic reticulum (ER) stress has been regarded as an important pathogenic component of type 2 diabetes. The possibility has been suggested that sulfonylurea, currently being used as one of the main oral hypoglycemic agents of type 2 diabetes, increases ER stress, which could lead to sulfonylurea failure. The authors of the present study examined ER stress of β-cells in a glucolipotoxic condition using glyburide (GB) in an environment mimicking type 2 diabetes.

Methods

Apoptosis was induced by adding various concentrations of GB (0.001 to 200 µM) to a glucolipotoxic condition using 33 mM glucose, and the effects of varied concentrations of palmitate were evaluated via annexin V staining. The markers of ER stress and pro-apoptotic markers were assessed by Western blotting and semi-quantitative reverse transcription-polymerase chain reaction. Additionally, the anti-apoptotic markers were evaluated.

Results

Addition of any concentration of GB in 150 µM palmitate and 33 mM glucose did not increase apoptosis. The expression of phosphorylated eukaryotic initiation factor (eIF-2α) was increased and cleaved caspase 3 was decreased by adding GB to a glucolipotoxic condition. However, other ER stress-associated markers such as Bip-1, X-box binding protein-1, ATF-4 and C/EBP-homologous protein transcription factor and anti-apoptotic markers phosphor-p85 phosphatidylinositol 3-kinase and phosphorylation of Akt did not change significantly.

Conclusion

GB did not show further deleterious effects on the degree of apoptosis or ER stress of INS-1 cells in a glucolipotoxic condition. Increased phosphorylation of eIF-2α may attenuate ER stress for adaptation to increased ER protein load.

Citations

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  • The antagonistic atorvastatin-glibenclamide interactions suppressed the atorvastatin-induced Bax/cytochrome c/p53 mRNA expressions and increased Rho A mRNA expression in B16f10 melanoma cell culture
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    Gene Reports.2021; 23: 101156.     CrossRef
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    International Journal of Molecular Sciences.2016; 17(2): 192.     CrossRef
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    Channels.2013; 7(6): 420.     CrossRef
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  • The Duration of Sulfonylurea Treatment Is Associated withβ-Cell Dysfunction in Patients with Type 2 Diabetes Mellitus
    Mi-Seon Shin, Jee Hee Yu, Chang Hee Jung, Jenie Yoonoo Hwang, Woo Je Lee, Min-Seon Kim, Joong-Yeol Park
    Diabetes Technology & Therapeutics.2012; 14(11): 1033.     CrossRef
The Effect of Glucose Fluctuation on Apoptosis and Function of INS-1 Pancreatic Beta Cells
Mi Kyung Kim, Hye Sook Jung, Chang Shin Yoon, Jung Hae Ko, Hae Jung Jun, Tae Kyun Kim, Min Jeong Kwon, Soon Hee Lee, Kyung Soo Ko, Byoung Doo Rhee, Jeong Hyun Park
Korean Diabetes J. 2010;34(1):47-54.   Published online February 28, 2010
DOI: https://doi.org/10.4093/kdj.2010.34.1.47
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AbstractAbstract PDFPubReader   
Background

Blood glucose level continuously fluctuates within a certain range in the human body. In diabetes patients, the extent of such fluctuation is large, despite the strict control of blood glucose. Blood glucose fluctuation has been shown to mediate more adverse effects on vascular endothelial cells and diabetes complications than chronic hyperglycemia, which has been explained as due to oxidative stress. As few previous studies have reported the effects of chronic and intermittent hyperglycemia on the apoptosis and function of pancreatic beta cells, this study reported herein was performed to investigate such effects on these cells.

Methods

For chronic hyperglycemia, INS-1 cells were cultured for 5 days with changes of RPMI 1640 medium containing 33 mM glucose every 12 hours. For intermittent hyperglycemia, the medium containing 11 mM glucose was exchanged with the medium containing 33 mM glucose every 12 hours. Apoptosis was assessed by TUNEL assay Hoechst staining and cleaved caspase 3. Insulin secretory capacity was assessed, and the expression of Mn-SOD and Bcl-2 was measured by Western blotting.

Results

In comparison to the control group, INS-1 cells exposed to chronic hyperglycemia and intermittent hyperglycemia showed an increase in apoptosis. The apoptosis of INS-1 cells exposed to intermittent hyperglycemia increased significantly more than the apoptosis of INS-1 cells exposed to chronic hyperglycemia. In comparison to the control group, the insulin secretory capacity in the two hyperglycemic states was decreased, and more with intermittent hyperglycemia than with chronic hyperglycemia. The expression of Mn-SOD and Bcl-2 increased more with chronic hyperglycemia than with intermittent hyperglycemia.

Conclusion

Intermittent hyperglycemia induced a higher degree of apoptosis and decreased the insulin secretory capacity more in pancreatic beta cells than chronic hyperglycemia. This activity may be mediated by the anti-oxidative enzyme Mn-SOD and the anti-apoptotic signal Bcl-2.

Citations

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  • Association between hemoglobin glycation index and diabetic kidney disease in type 2 diabetes mellitus in China: A cross- sectional inpatient study
    Sixu Xin, Xin Zhao, Jiaxiang Ding, Xiaomei Zhang
    Frontiers in Endocrinology.2023;[Epub]     CrossRef
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  • Correlation between HbA1c and Triglyceride Level with Coronary Stenosis Degree in Type 2 Diabetes Mellitus with Coronary Heart Disease
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    Open Access Macedonian Journal of Medical Sciences.2022; 10(B): 944.     CrossRef
  • Age‐specific associations of glycated haemoglobin variability with cardiovascular disease and mortality in patients with type 2 diabetes mellitus: A 10‐ year cohort study
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  • Molecular Mechanisms of Glucose Fluctuations on Diabetic Complications
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    You Jeong Kim, Su Min Park, Hye Sook Jung, Eun Ju Lee, Tae Kyoon Kim, Tae-Nyun Kim, Min Jeong Kwon, Soon Hee Lee, Byoung Doo Rhee, Mi-kyung Kim, Jeong Hyun Park
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Review
Impaired Wound Healing in Diabetes Mellitus.
Min Jeong Kwon, Jeong Hyun Park
Korean Diabetes J. 2009;33(2):83-90.   Published online April 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.2.83
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AbstractAbstract PDF
The normal healing of a cutaneous wound is achieved via well-orchestrated integration of complex biological and molecular events of cell migration, proliferation, extracellular matrix deposition and tissue remodeling. Chronic wounds fail to progress through the normal stages of healing, and enter a state of pathologic inflammation. Complicated diabetic patients show delayed wound healing caused by multiple factors including vascular insufficiency, abnormalities of the biochemical environment and hyperglycemia per se. Novel technologies including growth factor therapy, gene therapy, stem cell technologies, synthetic skins and hyperbaric oxygen treatment are under development. In the near future, these therapeutic strategies will be clinically available.

Citations

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    Han Na Lee, Jung Min Bae, Bon Cheol Leo Goo, Young Min Park
    Lasers in Medical Science.2019; 34(2): 421.     CrossRef
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    Jae Sung Hwang, Dae Il Sung, Whan Myung Lee, Young Shin Chung, Han Bok Kim
    The Korean Journal of Microbiology.2014; 50(3): 223.     CrossRef
  • Comparison of Outcome of Trabeculectomy With Mitomycin C and Ahmed Valve Implantation for Uveitic Glaucoma
    Joo Yeon Kim, Hyoung Sub Shim, Hwang Ki Kim, Yong Ho Sohn
    Journal of the Korean Ophthalmological Society.2010; 51(4): 575.     CrossRef
Editorial
Association Study of the Peroxisome Proliferators-Activated Receptor gamma2 Pro12Ala Polymorphism with Diabetic Nephropathy.
Min Jeong Kwon, Jeong Hyun Park
Korean Diabetes J. 2008;32(5):399-401.   Published online October 1, 2008
DOI: https://doi.org/10.4093/kdj.2008.32.5.399
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AbstractAbstract PDF
No abstract available.
Original Articles
Cloning of Novel Epidermal Growth Factor (EGF) Plasmid for Gene Therapy on Diabetic Foot Ulcer.
Hye Sook Chung, Chang Shin Yoon, Min Jeong Kwon, Mi Kyung Kim, Soon Hee Lee, Kyung Soo Ko, Byung Doo Rhee, Jeong Hyun Park
Korean Diabetes J. 2008;32(2):131-140.   Published online April 1, 2008
DOI: https://doi.org/10.4093/kdj.2008.32.2.131
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AbstractAbstract PDF
BACKGROUND
Epidermal Growth Factor (EGF) is one of the important growth factors involved in the epithelialization during cutaneous wound healing. Peptide EGF has been used for the treatment of diabetic foot ulcer. But the inferiority of cost-effectiveness and the inconvenience of daily application might have restricted its wide clinical usage. EGF gene therapy could dramatically improve the efficacy and inconvenience through long-term expression and bypassing the EGF degradation by hostile non-specific proteinases expressed in the wound bed. METHODS: EGF DNAs were amplified via PCR. For the more effective secretion from the transfected cell, we inserted furin cleavage site into EGF plasmids. The efficacy of novel plasmid pbeta-EGF was verified by transfection into the various animal cell lines, and the biologic potency of expressed EGF was confirmed via phosphorylation of PI3K and GSK3beta by Western blotting. RESULTS: We tested various kinds of human EGFs. One of the human EGF isoforms, EGF(828) including a membrane-anchoring domain was successfully released as the mature EGF protein in the cell culture media. Also EGF plasmid including furin cleavage site showed more than 2-fold increased EGF expression compared with the sequence without furin cleavage site. CONCLUSION: In conclusion, these findings suggest that mature EGF could be released easily out of cells by modifying EGF DNA sequence. Our novel EGF plasmid DNA could markedly increase the efficiency of non-viral gene therapy for diabetic foot ulcer.

Citations

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  • Effective healing of diabetic skin wounds by using nonviral gene therapy based on minicircle vascular endothelial growth factor DNA and a cationic dendrimer
    Min J. Kwon, Songhie An, Sunghyun Choi, Kihoon Nam, Hye S. Jung, Chang S. Yoon, Jung H. Ko, Hye J. Jun, Tae K. Kim, Soo J. Jung, Jeong H. Park, Yan Lee, Jong‐Sang Park
    The Journal of Gene Medicine.2012; 14(4): 272.     CrossRef
The Protective Effect of EGCG on INS-1 Cell in the Oxidative Stress and Mechanism.
Mi Kyung Kim, Hye Sook Jung, Chang Shin Yoon, Min Jeong Kwon, Kyung Soo Koh, Byung Doo Rhee, Jeong Hyun Park
Korean Diabetes J. 2008;32(2):121-130.   Published online April 1, 2008
DOI: https://doi.org/10.4093/kdj.2008.32.2.121
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AbstractAbstract PDF
BACKGROUND
Oxidative stress is important in both diabetic complications and the development and the progression of type 2 diabetes via the effects on the pancreatic beta-cells. EGCG (epigallocatechin galleate), a major constituent of green tea, has been known to have beneficial effects on various diseases through the mechanisms of antioxidant and cell signaling modulation. But, very small numbers of studies were published about the direct effects of EGCG on the pancreatic beta cell lines. We performed this study to see the protective effect of EGCG on pancreatic beta cell line under H2O2 and the mechanisms of this phenomenon. METHODS: We used INS-1 cells and hydrogen peroxide as an oxidative stressor. Their viabilities were verified by MTT assay and FACS. The activity of glutathione peroxidase was assessed by total glutathione quantification kit. Western blot and semi-quantitative RT-PCR for the catalase, SOD (superoxide dismutase), PI3K and Akt were performed. Functional status of INS-1 cells was tested by GSIS (glucose stimulated insulin secretion). RESULTS: The biological effects of EGCG were different according to its concentrations. 10 micrometer EGCG effectively protected hydrogen peroxide induced damage in INS-1 cells. The expression and the activity of SOD, catalase and the glutathione peroxidase were significantly increased by EGCG. EGCG significantly increased PI3K and Akt activity and its effect was inhibited partially by wortmannin. GSIS was well preserved by EGCG. CONCLUSION: EGCG in low concentration effectively protected INS-1 cells from the oxidative stress through the activation of both antioxidant systems and anti-apoptosis signaling. Further studies will be necessary for the more detailed mechanisms and the clinical implications.

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Cytoprotective Effect by Antioxidant Activity of Quercetin in INS-1 Cell Line.
Min Jeong Kwon, Hye Sook Jung, Mi Kyung Kim, Seong Hoon Kang, Gwang Wook Seo, Jae Kwang Song, Tae Yeon Yoon, Min Kyeong Jeon, Tae Hwan Ha, Chang Shin Yoon, Mi Kyung Kim, Woo Je Lee, Jeong Hyun Noh, Soo Kyung Kwon, Dong Joon Kim, Kyung Soo Koh, Byung Doo Rhee, Kyung Ho Lim, Soon Hee Lee, Jeong Hyun Park
Korean Diabetes J. 2007;31(5):383-390.   Published online September 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.5.383
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AbstractAbstract PDF
BACKGROUND
Oxidative stress is induced under diabetic conditions and causes various forms of tissue damages in the patients with diabetes. Recently, pancreatic beta cells are regarded as a putative target of oxidative stress-induced tissue damage, and this seems to explain in part the progressive deterioration of beta cell function in type 2 diabetes. The aim of this study was to examine the potential of Quercetin (QE) to protect INS-1 cells from the H2O2-induced oxidative stress and the effects of QE on the glucose-stimulated insulin secretion in INS-1 cells. METHODS: To study the cell viability, cells were incubated with H2O2 and/or QE at the various concentrations. To confirm the protective effect by QE in response to H2O2, the levels of antioxidant enzymes were assessed by RT-PCR and Western blot, and glutathione peroxidase activities were quantified by spectrophotometrical method. Glucose-stimulated insulin secretion (GSIS) was measured by ELISA. RESULTS: Cell incubations were performed with 80 microM of H2O2 for 5 hours to induce 40 - 50% of cell death. QE gradually showed protective effect (IC50 = 50 microM) in dose-dependent manner. Superoxide dismutase (SOD) mRNA level in H2O2 + QE group was increased as compared to H2O2 group, but catalase did not changed. And the QE recruited glutathione peroxidase activity against H2O2-induced oxidative injuries in INS-1 cells. CONCLUSION: In conclusion, these findings suggest that QE might have protective effect on beta cells by ameliorating oxidative stress and preserving insulin secretory function.

Citations

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    Korean Journal of Food Preservation.2015; 22(1): 134.     CrossRef
  • Protective Effects of Sasa Borealis Leaves Extract on High Glucose-Induced Oxidative Stress in Human Umbilical Vein Endothelial Cells
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    Journal of the Korean Society of Food Science and Nutrition.2010; 39(12): 1753.     CrossRef

Diabetes Metab J : Diabetes & Metabolism Journal