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      Lipopolysaccharide에 의한 심장조직의 염증 반응과 심근 기능 이상에 대한 fenofibrate의 조절 효과 = Regulatory Effects of Fenofibrate with Inflammatory Response and Myocardiac Dysfunction in Lipopolysaccharidestimulated Heart Tissues

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      https://www.riss.kr/link?id=A104607820

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      다국어 초록 (Multilingual Abstract)

      Purpose: This study was intended to establish experimental conditions for monitoring the cardioprotective effects of fenofibrate on cardiac function in lipopolysaccharide (LPS)-stimulated BalB/c mice.
      Methods: To investigate the effects of fenofibrate on cardiac function, expression of Peroxisome proliferator-activated receptors (PPARs) and Peroxisome proliferator-activated receptor Gamma coactivator 1(PGC-1) and its target gene in the heart tissues of mice was compared after controls and LPS injection with pretreated fenofibrate or alone using Reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot analysis, and immunohistochemistry.
      In addition, Enzyme-linked-immunosorbent-assays (ELISA) were performed for assessment of pro-inflammatory cytokines of blood serum.
      Results: Pretreated with fenofibrate had protective effects of diminishing the levels of LPS-induced pro-inflammatory cytokines, including interleukin-1β(IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α(TNF-α) and recovery from reduction of messenger Ribo-nucleic acid, protein level of PPARs and PGC-1 in LPS-administered heart tissue. In addition, increasing expression of PPARs and PGC-1 ameliorated the expression and activity of catalase blocked production of lipid peroxidation.
      Conclusion: Treatment with fenofibrate resulted in augmented expression of transcription factors and reduced production of pro-inflammatory cytokines and lipid peroxidation after LPS administration. Therefore, results of this study suggested that fenofibrate should not only have a protective effect but should also restore cardiac function in several cardiac dysfunctional situations.
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      Purpose: This study was intended to establish experimental conditions for monitoring the cardioprotective effects of fenofibrate on cardiac function in lipopolysaccharide (LPS)-stimulated BalB/c mice. Methods: To investigate the effects of fenofibrate...

      Purpose: This study was intended to establish experimental conditions for monitoring the cardioprotective effects of fenofibrate on cardiac function in lipopolysaccharide (LPS)-stimulated BalB/c mice.
      Methods: To investigate the effects of fenofibrate on cardiac function, expression of Peroxisome proliferator-activated receptors (PPARs) and Peroxisome proliferator-activated receptor Gamma coactivator 1(PGC-1) and its target gene in the heart tissues of mice was compared after controls and LPS injection with pretreated fenofibrate or alone using Reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot analysis, and immunohistochemistry.
      In addition, Enzyme-linked-immunosorbent-assays (ELISA) were performed for assessment of pro-inflammatory cytokines of blood serum.
      Results: Pretreated with fenofibrate had protective effects of diminishing the levels of LPS-induced pro-inflammatory cytokines, including interleukin-1β(IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α(TNF-α) and recovery from reduction of messenger Ribo-nucleic acid, protein level of PPARs and PGC-1 in LPS-administered heart tissue. In addition, increasing expression of PPARs and PGC-1 ameliorated the expression and activity of catalase blocked production of lipid peroxidation.
      Conclusion: Treatment with fenofibrate resulted in augmented expression of transcription factors and reduced production of pro-inflammatory cytokines and lipid peroxidation after LPS administration. Therefore, results of this study suggested that fenofibrate should not only have a protective effect but should also restore cardiac function in several cardiac dysfunctional situations.

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      참고문헌 (Reference)

      1 Akira S, "Toll-like receptors: critical proteins linking innate and acquired immunity" 2 : 675-680, 2001

      2 Beigneux AP, "The acute phase response is associated with retinoid X receptor repression in rodent liver" 275 : 16390-16399, 2000

      3 Willson TM, "The PPARs: from orphan receptors to drug discovery" 43 : 527-550, 2000

      4 Schrader M, "Peroxisomes and oxidative stress" 1763 : 1755-1766, 2006

      5 Huss JM, "Peroxisome proliferatoractivated receptor coactivator-1alpha (PGC-1alpha) coactivates the cardiac-enriched nuclear receptors estrogenrelated receptor-alpha and -gamma. Identification of novel leucine-rich interaction motif within PGC-1alpha" 277 : 40265-40274, 2002

      6 Lehman JJ, "Peroxisome proliferator-activated receptor gamma coactivator-1 promotes cardiac mitochondrial biogenesis" 106 : 847-856, 2000

      7 Drew PD, "Peroxisome proliferator-activated receptor agonist regulation of glial activation: relevance to CNS inflammatory disorders" 49 : 183-189, 2006

      8 Lazarow PB, "Peroxisome biogenesis: advances and conundrums" 15 : 489-497, 2003

      9 Barger PM, "PPAR signaling in the control of cardiac energy metabolism" 10 : 238-245, 2000

      10 Maitra U, "Molecular mechanism underlying the suppression of lipid oxidation during endotoxemia" 47 : 420-425, 2009

      1 Akira S, "Toll-like receptors: critical proteins linking innate and acquired immunity" 2 : 675-680, 2001

      2 Beigneux AP, "The acute phase response is associated with retinoid X receptor repression in rodent liver" 275 : 16390-16399, 2000

      3 Willson TM, "The PPARs: from orphan receptors to drug discovery" 43 : 527-550, 2000

      4 Schrader M, "Peroxisomes and oxidative stress" 1763 : 1755-1766, 2006

      5 Huss JM, "Peroxisome proliferatoractivated receptor coactivator-1alpha (PGC-1alpha) coactivates the cardiac-enriched nuclear receptors estrogenrelated receptor-alpha and -gamma. Identification of novel leucine-rich interaction motif within PGC-1alpha" 277 : 40265-40274, 2002

      6 Lehman JJ, "Peroxisome proliferator-activated receptor gamma coactivator-1 promotes cardiac mitochondrial biogenesis" 106 : 847-856, 2000

      7 Drew PD, "Peroxisome proliferator-activated receptor agonist regulation of glial activation: relevance to CNS inflammatory disorders" 49 : 183-189, 2006

      8 Lazarow PB, "Peroxisome biogenesis: advances and conundrums" 15 : 489-497, 2003

      9 Barger PM, "PPAR signaling in the control of cardiac energy metabolism" 10 : 238-245, 2000

      10 Maitra U, "Molecular mechanism underlying the suppression of lipid oxidation during endotoxemia" 47 : 420-425, 2009

      11 Doenst T, "Load-induced changes in vivo alter substrate fluxes and insulin responsiveness of rat heart in vitro" 50 : 1083-1090, 2001

      12 Vodovotz Y, "Inducible nitric oxide synthase in tanglebearing neurons of patients with Alzheimer's disease" 184 : 1425-1433, 1996

      13 Gervois P, "Global suppression of IL-6-induced acute phase response gene expression after chronic in vivo treatment with the peroxisome proliferator-activated receptoralpha activator fenofibrate" 279 : 16154-16160, 2004

      14 Zhang Y, "Estrogen-related receptors stimulate pyruvate dehydrogenase kinase isoform 4 gene expression" 281 : 39897-39906, 2006

      15 Huss JM, "Estrogen-related receptor alpha directs peroxisome proliferator- activated receptor alpha signaling in the transcriptional control of energy metabolism in cardiac and skeletal muscle" 24 : 9079-9091, 2004

      16 Khan M, "Endotoxin-induced alterations of lipid and fatty acid compositions in rat liver peroxisomes" 6 : 41-50, 2000

      17 Wang X, "Effect of endotoxin and platelet-activating factor on lipid oxidation in the rat heart" 29 : 1915-1926, 1997

      18 Bone RC, "Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis" American College of Chest Physicians/Society of Critical Care Medicine 101 : 1644-1655, 1992

      19 Balligand JL, "Control of cardiac muscle cell function by an endogenous nitric oxide signaling system" 90 : 347-351, 1993

      20 Fallach R, "Cardiomyocyte Toll-like receptor 4 is involved in heart dysfunction following septic shock or myocardial ischemia" 48 : 1236-1244, 2010

      21 Balligand JL, "Abnormal contractile function due to induction of nitric oxide synthesis in rat cardiac myocytes follows exposure to activated macrophage-conditioned medium" 91 : 2314-2319, 1993

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      연월일 이력구분 이력상세 등재구분
      2027 평가예정 재인증평가 신청대상 (재인증)
      2021-01-01 평가 등재학술지 유지 (재인증) KCI등재
      2020-05-08 학회명변경 영문명 : The Korean Society Of Emergency Medicine -> The Korean Society of Emergency Medicine KCI등재
      2018-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2015-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2006-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2005-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2003-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.23 0.23 0.22
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.22 0.22 0.339 0.06
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