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      Glucose-Insulin-Potassium Solution Protects Ventricular Myocytes of Neonatal Rat in an In Vitro Coverslip Ischemia/Reperfusion Model

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      https://www.riss.kr/link?id=A104685762

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      다국어 초록 (Multilingual Abstract)

      Background and Objectives: The benefit of high glucose-insulin-potassium (GIK) solution in clinical applications is controversial. We established a neonatal rat ventricular myocyte (NRVM) in vitro coverslip ischemia/reperfusion (I/R) model and investigated the effects of GIK solution on suppressing reactive oxygen species (ROS) and upregulating O -GlcNacylation, which protects cells from ischemic injury.
      Materials and Methods: NRVMs were isolated from postnatal day 3–4 Sprague–Dawley rat pups and grown in Dulbecco’s modified Eagle’s medium containing high glucose (4.5 g/L), fetal bovine serum, and penicillin/streptomycin. The effects of the GIK solution on ROS production, apoptosis, and expression of O -GlcNAc and O -GlcNAc transferase (OGT) were investigated in the coverslip I/R model.
      Results: Covering the 24-well culture plates for 3 hr with 12 mm diameter coverslips resulted in the appropriate ischemic shock. Glucose and insulin synergistically reduced ROS production, protected NRVM dose-dependently from apoptosis, and altered O -GlcNAc and OGT expression.
      Conclusion: The high GIK solution protected NRVM from I/R injury in vitro by reducing ROS and altering O- GlcNacylation.
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      Background and Objectives: The benefit of high glucose-insulin-potassium (GIK) solution in clinical applications is controversial. We established a neonatal rat ventricular myocyte (NRVM) in vitro coverslip ischemia/reperfusion (I/R) model and investi...

      Background and Objectives: The benefit of high glucose-insulin-potassium (GIK) solution in clinical applications is controversial. We established a neonatal rat ventricular myocyte (NRVM) in vitro coverslip ischemia/reperfusion (I/R) model and investigated the effects of GIK solution on suppressing reactive oxygen species (ROS) and upregulating O -GlcNacylation, which protects cells from ischemic injury.
      Materials and Methods: NRVMs were isolated from postnatal day 3–4 Sprague–Dawley rat pups and grown in Dulbecco’s modified Eagle’s medium containing high glucose (4.5 g/L), fetal bovine serum, and penicillin/streptomycin. The effects of the GIK solution on ROS production, apoptosis, and expression of O -GlcNAc and O -GlcNAc transferase (OGT) were investigated in the coverslip I/R model.
      Results: Covering the 24-well culture plates for 3 hr with 12 mm diameter coverslips resulted in the appropriate ischemic shock. Glucose and insulin synergistically reduced ROS production, protected NRVM dose-dependently from apoptosis, and altered O -GlcNAc and OGT expression.
      Conclusion: The high GIK solution protected NRVM from I/R injury in vitro by reducing ROS and altering O- GlcNacylation.

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      참고문헌 (Reference)

      1 Ngoh GA, "Unique hexosaminidase reduces metabolic survival signal and sensitizes cardiac myocytes to hypoxia/reoxygenation injury" 104 : 41-49, 2009

      2 Laybutt DR, "Selective chronic regulation of GLUT1 and GLUT4 content by insulin, glucose and lipid in rat cardiac muscle in vivo" 273 : H1309-H1316, 1997

      3 Oliver MF, "Relation between serum-freefatty acids and arrhythmias and death after acute myocardial infarction" 1 : 710-714, 1968

      4 Darley-Usmar VM, "Protein O-linked β-Nacetylglucosamine:a novel effector of cardiomyocyte metabolism and function" 52 : 538-549, 2012

      5 Murry CE, "Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium" 74 : 1124-1136, 1986

      6 Jovic M, "Preconditioning with glucose-insulin-potassium solution and restoration of myocardial function during coronary surgery" 28 : 262-270, 2009

      7 Thibault H, "Postconditioning the human heart" 37 : 19-22, 2007

      8 Rohr S, "Patterned growth of neonatal rat heart cells in culture. Morphological and electrophysiological characterization" 68 : 114-130, 1991

      9 Rasoul S, "One year outcomes after glucose-insulin-potassium in ST elevation myocardial infarction. The Glucose-insulin-potassium study II" 122 : 52-55, 2007

      10 Hart GW, "O-GlcNAcylation of key nuclear and cytoskeletal proteins: reciprocity with O-phosphorylation and putative roles in protein multimerization" 6 : 711-716, 1996

      1 Ngoh GA, "Unique hexosaminidase reduces metabolic survival signal and sensitizes cardiac myocytes to hypoxia/reoxygenation injury" 104 : 41-49, 2009

      2 Laybutt DR, "Selective chronic regulation of GLUT1 and GLUT4 content by insulin, glucose and lipid in rat cardiac muscle in vivo" 273 : H1309-H1316, 1997

      3 Oliver MF, "Relation between serum-freefatty acids and arrhythmias and death after acute myocardial infarction" 1 : 710-714, 1968

      4 Darley-Usmar VM, "Protein O-linked β-Nacetylglucosamine:a novel effector of cardiomyocyte metabolism and function" 52 : 538-549, 2012

      5 Murry CE, "Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium" 74 : 1124-1136, 1986

      6 Jovic M, "Preconditioning with glucose-insulin-potassium solution and restoration of myocardial function during coronary surgery" 28 : 262-270, 2009

      7 Thibault H, "Postconditioning the human heart" 37 : 19-22, 2007

      8 Rohr S, "Patterned growth of neonatal rat heart cells in culture. Morphological and electrophysiological characterization" 68 : 114-130, 1991

      9 Rasoul S, "One year outcomes after glucose-insulin-potassium in ST elevation myocardial infarction. The Glucose-insulin-potassium study II" 122 : 52-55, 2007

      10 Hart GW, "O-GlcNAcylation of key nuclear and cytoskeletal proteins: reciprocity with O-phosphorylation and putative roles in protein multimerization" 6 : 711-716, 1996

      11 Ngoh GA, "Non-canonical glycosyltransferase modulates post-hypoxic cardiac myocyte death and mitochondrial permeability transition" 45 : 313-325, 2008

      12 Yellon DM, "Myocardial reperfusion injury" 357 : 1121-1135, 2007

      13 Ji L, "Insulin attenuates myocardial ischemia/reperfusion injury via reducing oxidative/nitrative stress" 298 : E871-E880, 2010

      14 Obeid AI, "Influence of glucose, insulin, and potassium on vulnerability to ventricular fibrillation in the canine heart" 43 : 601-608, 1978

      15 Brown MJ, "Hypokalemia from beta2-receptor stimulation by circulating epinephrine" 309 : 1414-1419, 1983

      16 Diaz R, "Glucose-insulin-potassium therapy in patients with ST-segment elevation myocardial infarction" 298 : 2399-2405, 2007

      17 Grossman AN, "Glucose-insulin-potassium revived: current status in acute coronary syndromes and the energy-depleted heart" 127 : 1040-1048, 2013

      18 Howell NJ, "Glucose-insulin-potassium reduces the incidence of low cardiac output episodes after aortic valve replacement for aortic stenosis in patients with left ventricular hypertrophy: results from the Hypertrophy, Insulin, Glucose and Electrolytes (HINGE) trial" 123 : 170-177, 2011

      19 Apstein CS, "Glucose-insulin-potassium in acute myocardial infarction: the time has come for a large, prospective trial" 96 : 1074-1077, 1997

      20 Champattanachai V, "Glucosamine protects neonatal cardiomyocytes from ischemia-reperfusion injury via increased protein-associated O-GlcNAc" 292 : C178-C187, 2007

      21 Carbó R, "Effects of polarizing solution on glucose uptake of rat oxygenated or hypoxic ventricular myocytes" 30 : 64-71, 2003

      22 Krljanac G, "Effects of glucose-insulin-potassium infusion on ST-elevation myocardial infarction in patients treated with thrombolytic therapy" 96 : 1053-1058, 2005

      23 Oliver EMF, "Effects of glucose and fatty acids on myocardial ischemia and arrhythmias" 343 : 155-158, 1994

      24 Sodi-Pallares D, "Effects of an intravenous infusion of a potassium-glucose-insulin solution on the electrocardiographic signs of myocardial infarction. A preliminary clinical report" 9 : 166-181, 1962

      25 Mehta SR, "Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-segment elevation myocardial infarction: the CREATE-ECLA randomized controlled trial" 293 : 437-446, 2005

      26 Zachara NE, "Dynamic O-GlcNAc modification of nucleocytoplasmic proteins in response to stress. A survival response of mammalian cells" 279 : 30133-30142, 2004

      27 Pitts KR, "Coverslip hypoxia: a novel method for studying cardiac myocyte hypoxia and ischemia in vitro" 287 : H1801-H1812, 2004

      28 Yusuf S, "Challenges in the conduct of large simple trials of important generic questions in resource-poor settings:the CREATE and ECLA trial program evaluating GIK (glucose, insulin and potassium) and low-molecular-weight heparin in acute myocardial infarction" 148 : 1068-1078, 2004

      29 Cave AC, "ATP synthesis during low-flow ischemia: influence of increased glycolytic substrate" 101 : 2090-2096, 2000

      30 문일수, "A Simple Method for Combined Fluorescence In Situ Hybridization and Immunocytochemistry" 한국분자세포생물학회 24 (24): 76-82, 2007

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      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2008-05-15 학회명변경 한글명 : 대한순환기학회 -> 대한심장학회
      영문명 : The Korean Society Of Circulation -> The Korean Society of Cardiology
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      2007-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2005-08-02 학술지등록 한글명 : Korean Circulation Journal
      외국어명 : Korean Circulation Journal
      KCI등재
      2004-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2003-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2001-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 1.13 0.34 0.71
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.45 0.36 0.52 0.12
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