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      NF-κB 활성 저해를 통한 대두 유래 Peptide의 Cycooxygenase-2 발현 및 Prostalandin E2 생성의 억제 = Inhibition of Cyclooxygenase-2 Activity and Prostaglandin E2 Production through Down-regulation of NF-κB Activity by Peptide Derived from Soy Bean

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      https://www.riss.kr/link?id=A104794564

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      다국어 초록 (Multilingual Abstract)

      Frequent consumption of soy and soy-based products is associated with reduced inflammation and
      cancer incidence. Pro-inflammatory mediators, such as prostaglandin E2 (PGE2) and cyclooxygenases-2
      (COX-2), play pivotal roles in normal as well as transformed cells. In this study, we examined the effect
      of peptide [Leu-Leu-Pro-His-His (LLPHH)] derived from soy bean on phorbol 12-myristate 13-acetate
      (PMA)-induced inflammatory responses using human lymphatic U937 cell model. Treatment of PMA
      significantly induced COX-2 expression and PGE2 production in U937 cells. However, the pretreatment
      with LLPHH markedly inhibited the PMA-induced COX-2 expression as well as PGE2 production in a
      dose-dependent manner. Moreover, the LLPHH prevented the nuclear translocation of nuclear factor
      kappaB (NF-κB p65) stimulated by PMA treatment. However, the elevated levels of early growth
      response gene-1 (Egr-1) expression by PAM were not reduced by the pretreatment of LLPHH. Taken
      together, the present data indicate that the LLPHH derived from soy bean exhibits anti-inflammatory
      properties by suppressing the transcription of pro-inflammatory cytokine genes through the NF-kB
      signaling pathway. These findings support the hypothesis that the soy peptides reduce the risk of
      tumorigenesis possibly by suppressing inflammatory responses. (Cancer Prev Res 13, 233-241, 2009)
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      Frequent consumption of soy and soy-based products is associated with reduced inflammation and cancer incidence. Pro-inflammatory mediators, such as prostaglandin E2 (PGE2) and cyclooxygenases-2 (COX-2), play pivotal roles in normal as well as transfo...

      Frequent consumption of soy and soy-based products is associated with reduced inflammation and
      cancer incidence. Pro-inflammatory mediators, such as prostaglandin E2 (PGE2) and cyclooxygenases-2
      (COX-2), play pivotal roles in normal as well as transformed cells. In this study, we examined the effect
      of peptide [Leu-Leu-Pro-His-His (LLPHH)] derived from soy bean on phorbol 12-myristate 13-acetate
      (PMA)-induced inflammatory responses using human lymphatic U937 cell model. Treatment of PMA
      significantly induced COX-2 expression and PGE2 production in U937 cells. However, the pretreatment
      with LLPHH markedly inhibited the PMA-induced COX-2 expression as well as PGE2 production in a
      dose-dependent manner. Moreover, the LLPHH prevented the nuclear translocation of nuclear factor
      kappaB (NF-κB p65) stimulated by PMA treatment. However, the elevated levels of early growth
      response gene-1 (Egr-1) expression by PAM were not reduced by the pretreatment of LLPHH. Taken
      together, the present data indicate that the LLPHH derived from soy bean exhibits anti-inflammatory
      properties by suppressing the transcription of pro-inflammatory cytokine genes through the NF-kB
      signaling pathway. These findings support the hypothesis that the soy peptides reduce the risk of
      tumorigenesis possibly by suppressing inflammatory responses. (Cancer Prev Res 13, 233-241, 2009)

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      참고문헌 (Reference)

      1 Sarkar A, "β-Dglucoside suppresses tumor necrosis factor-induced activation of nuclear transcription factor kappaB but potentiates apoptosis" 279 : 33768-33781, 2004

      2 Lee E, "α-tocopheryl succinate, in contrast to α-tocopherol and α-tocopheryl acetate, inhibits prostaglandin E2 production in human lung epithelial cells" 27 : 2308-2315, 2006

      3 Botting RM, "selectivity and uses.J Physiol Pharmacol 57" 57 : 113-124, 2006

      4 Heuze-Vourc'h N, "an antiangiogenic cytokine that inhibits COX-2 expression" 333 : 470-475, 2005

      5 Rabe KF, "Update in chronic obstructive pulmonary disease" 175 : 1222-1232, 2006

      6 Yamamoto Y, "Therapeutic potential of inhibition of the NF-κB pathway in the treatment of inflammation and cancer" 107 : 135-142, 2007

      7 Seo YJ, "The effects of phorbol 12-myristate 13-acetate, cholera toxin, prostaglandin E2 and norepinephrine on inducible nitric oxide synthase activation induced by lipopolysaccharide in C6 cells" 78 : 178-184, 2006

      8 Chen KH, "Tangeretin suppresses IL-1β- induced cyclooxygenase (COX)-2 expression through inhibition of p38 MAPK, JNK, and AKT activation in human lung carcinoma cells" 73 : 215-227, 2007

      9 Yucel-Lindberg T, "Signal pathways involved in the regulation of prostaglandin E synthase-1 in human gingival fibroblasts" 18 : 2131-2142, 2006

      10 de Souza Pereira R, "Selective cyclooxygenase-2 (COX-2)inhibitors used for preventing or regressing cancer" 4 : 157-163, 2009

      1 Sarkar A, "β-Dglucoside suppresses tumor necrosis factor-induced activation of nuclear transcription factor kappaB but potentiates apoptosis" 279 : 33768-33781, 2004

      2 Lee E, "α-tocopheryl succinate, in contrast to α-tocopherol and α-tocopheryl acetate, inhibits prostaglandin E2 production in human lung epithelial cells" 27 : 2308-2315, 2006

      3 Botting RM, "selectivity and uses.J Physiol Pharmacol 57" 57 : 113-124, 2006

      4 Heuze-Vourc'h N, "an antiangiogenic cytokine that inhibits COX-2 expression" 333 : 470-475, 2005

      5 Rabe KF, "Update in chronic obstructive pulmonary disease" 175 : 1222-1232, 2006

      6 Yamamoto Y, "Therapeutic potential of inhibition of the NF-κB pathway in the treatment of inflammation and cancer" 107 : 135-142, 2007

      7 Seo YJ, "The effects of phorbol 12-myristate 13-acetate, cholera toxin, prostaglandin E2 and norepinephrine on inducible nitric oxide synthase activation induced by lipopolysaccharide in C6 cells" 78 : 178-184, 2006

      8 Chen KH, "Tangeretin suppresses IL-1β- induced cyclooxygenase (COX)-2 expression through inhibition of p38 MAPK, JNK, and AKT activation in human lung carcinoma cells" 73 : 215-227, 2007

      9 Yucel-Lindberg T, "Signal pathways involved in the regulation of prostaglandin E synthase-1 in human gingival fibroblasts" 18 : 2131-2142, 2006

      10 de Souza Pereira R, "Selective cyclooxygenase-2 (COX-2)inhibitors used for preventing or regressing cancer" 4 : 157-163, 2009

      11 Ghosh M, "Role of cytosolic phospholipase A(2) in prostaglandin E(2) production by lung fibroblasts" 30 : 91-100, 2004

      12 Tong M, "Reciprocal regulation of cyclooxygenase- 2 and 15-hydroxyprostaglandin dehydrogenase expression in A549 human lung adenocarcinoma cells" 27 : 2170-2109, 2006

      13 Rosch S, "Prostaglandin E2 inducescyclooxygenase-2 expression in human nonpigmented ciliary epithelial cells through activation of p38 and p42/44 mitogen-activated protein kinases" 338 : 1191-1178, 2005

      14 Kramer EL, "Perinatal increases in TGF-α disrupt the saccular phase of lung morphogenesis and cause remodeling: microarray analysis" 293 : L314-L327, 2007

      15 Surh YJ, "Molecular mechanisms underlying chemopreventive activities of anti-inflammatory phytochemicals: down-regulation of COX-2 and iNOS through suppression of NF-κB activation" 480 : 243-268, 2001

      16 Wymann MP, "Lipid signalling in disease" 9 : 162-176, 2008

      17 Vainio H, "Is COX-2 inhibition a panacea for cancer prevention?" 94 : 613-614, 2001

      18 Moon Y, "Involvement of early growth response gene 1 in the modulation of microsomal prostaglandin E synthase 1 by epigallocatechin gallate in A549 human pulmonary epithelial cells" 73 : 125-135, 2007

      19 Nieminen R, "Inhibitors of mitogen-activated protein kinases downregulate COX-2 expression in human chondrocytes" 2005 : 247-255, 2005

      20 Takada Y, "Indole-3-carbinol suppresses NF-κB and IκBα kinase activation, causing inhibition of expression of NF-κB-regulated antiapoptotic and metastatic gene products and enhancement of apoptosis in myeloid and leukemia cells" 106 : 641-649, 2005

      21 Murakami A, "INOS and COX-2 in inflammatory cells: chemoprevention using food phytochemicals" 121 : 2357-2363, 2007

      22 Xu W, "FP prostanoid receptor-mediated induction of the expression of early growth response factor-1 by activation of a Ras/ Raf/mitogen-activated protein kinase signaling cascade" 73 : 111-118, 2008

      23 Creminon C, "Differential measurement of constitutive (COX-1) and inducible (COX-2) cyclooxygenase expression in human umbilical vein endothelial cells using specific immunometric enzyme immunoassays" 1254 : 341-348, 1995

      24 30)Faour WH,Alaaeddine N,Mancini A,He QW,Jovanovic D, "Di Battista JA.Early growth response factor-1 mediates prostaglandin E2-dependent transcriptional suppression of cytokineinduced tumor necrosis factor-α gene expression in human macrophages and rheumatoid arthritis-affected synovial fibroblasts.J Biol Chem 280" 9536-9546 2005

      25 Dempke W, "Cyclooxygenase- 2: a novel target for cancer chemotherapy?" 127 : 411-417, 2001

      26 Brunelle M, "Cyclooxygenase- 2 expression in normal and neoplastic canine mammary cell lines" 43 : 656-666, 2006

      27 Sawaoka H, "Cyclooxygenase inhibitors suppress angiogenesis and reduce tumor growth in vivo" 79 : 1649-1477, 1999

      28 조재위, "Curcumin inhibits the expression of COX-2 in UVB-irradiated human keratinocytes (HaCaT) by inhibiting activation of AP-1: p38 MAP kinase and JNK as potential upstream targets" 생화학분자생물학회 37 (37): 186-192, 2005

      29 Jin DZ, "Cryptotanshinone inhibits cyclooxygenase-2 enzyme activity but not its expression" 549 : 166-172, 2006

      30 Lev-Ari S, "Compositions for treatment of cancer and inflammation" 3 : 55-62, 2008

      31 Reynolds PR, "Cigarette smoke-induced Egr-1 upregulates pro-inflammatory cytokines in pulmonary epithelial cells" 35 : S314-S319, 2006

      32 Soodvilai S, "Acute regulation of OAT3-mediated estrone sulfate transport in isolated rabbit renal proximal tubules" 287 : F1021-F1029, 2004

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2022 평가예정 재인증평가 신청대상 (재인증)
      2019-01-01 평가 등재학술지 선정 (계속평가) KCI등재
      2018-12-01 평가 등재후보로 하락 (계속평가) KCI등재후보
      2015-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2013-10-14 학술지명변경 외국어명 : Cancer Prevention Research -> Journal of Cancer Prevention KCI등재
      2012-10-15 학회명변경 영문명 : Korean Association of Cancer Prevention -> Korean Society of Cancer Preveniton KCI등재
      2011-04-04 학술지명변경 외국어명 : Journal of Korean Association of Cancer Prevention -> Cancer Prevention Research KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2008-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2007-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2005-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.22 0.22 0.18
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.15 0.12 0.405 0.13
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