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The mechanism of endotoxin-induced vascular endothelial injury

The mechanism of endotoxin-induced vascular endothelial injury
内毒素引起血管内皮损伤的机制
批准号:
11670278
负责人:
YOKOCHI Takashi
金额:
$2.43万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1999
资助国家:
日本
项目状态:
已结题
起止时间:
1999 至 2000

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中文摘要
翻译
研究了干扰素-γ (IFN-γ)、肿瘤坏死因子-α (TNF-α)和脂多糖(LPS)对小鼠血管主动脉内皮细胞系END-D一氧化氮(NO)生成的影响。LPS、TNF-α和较低浓度IFN-γ均抑制END-D细胞NO的产生,而较高浓度IFN-γ则明显促进其产生。高浓度IFN-γ诱导的NO生成在LPS或TNF-α联合作用下进一步增强。在LPS和IFN-γ的连续孵育中,NO生成的增强需要预先用IFN-γ处理。高浓度IFN-γ刺激END-D细胞导致诱导型NO合成酶(iNOS)的表达。IFN-γ单独或与LPS或TNF-α联合增加NO的产生被几种iNOS抑制剂完全阻断。结果表明,较高浓度的IFN-γ本身通过iNOS的表达增强了END-D细胞中NO的产生。LPS和TNF-α单独调节曾被IFN-γ触发的iNOS活性。另一方面,较低浓度的IFN-γ。LPS和TNF-α通过下调一氧化氮的组成型来减少一氧化氮的产生,提示促炎因子可能通过一氧化氮的产生参与了LPS诱导的血管内皮损伤。
英文摘要
Effect of interferon-gamma(IFN-γ), tumor-necrosis factor-alpha(TNF-α)and lipopolysaccharide(LPS)on nitric oxide(NO)production in mouse vascular aortic endothelial cell line END-D was examined. LPS, TNF-α, and a lower concentration of IFN-γ inhibited NO production in END-D cells, while a higher concentration of IFN-γ definitely enhanced it. The NO production induced by a high concentration of IFN-γ was further augmented in combination with LPS or TNF-α. In the sequential incubation of LPS and IFN-γ, the enhancement of NO production required the prior treatment with IFN-γ. Stimulation of END-D cells with a high concentration of IFN-γ led to the expression of inducible type NO synthase(iNOS). The augmentation of NO production by IFN-γ alone or in combination with LPS or TNF-α was completely blocked by several inhibitors of iNOS.It was strongly suggested that a higher concentration of IFN-γ itself enhanced NO production in END-D cells through the expression of iNOS.LPS and TNF-α exclusively modulated the activity of iNOS which expression was once tiggered by IFN-γ. On the other hand, a lower concentration of IFN-γ.LPS and TNF-α reduced NO production through down-regulating constitutive type NOS.It was suggested that proinflammatory cytokines may be involved in LPS-induced vascular endothelial injury via NO production.
期刊论文(10)
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科研奖励(0)
会议论文
D.Chakravortty, Y.Kato, N.Koide, T.Sugiyama, M.Kawai, M.Fukada, T.Yoshida, T.Yokochi.: "Production of tissue factor in CD14-expressing human umbilical vein endothelial cells by lipopolysaccharide."FEMS Microbiol.Lett.. 178. 235-239 (1999)
D.Chakravortty、Y.Kato、N.Koide、T.Sugiyama、M.Kawai、M.Fukada、T.Yoshida、T.Yokochi.:“通过脂多糖在表达 CD14 的人脐静脉内皮细胞中产生组织因子。
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通讯作者:
Y.Kato,T.Yokochi, et.al.: "Big mitogen-activated kinase regulates multiple members of the MEF2 protein family."J.Biol.Chem.. 275. 18534-18540 (2000)
Y.Kato,T.Yokochi, et.al.:“大丝裂原激活激酶调节 MEF2 蛋白家族的多个成员。”J.Biol.Chem.. 275. 18534-18540 (2000)
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通讯作者:
A.Morikawa,T.Yokochi. et.al.: "Augmentation of nitric oxide production by interferon-γin mouse vascular endothelial cell line and its modulation by tumor necrosis factor-α and lipopolysaccharide."Infect.Immun.. 68. 6209-6214 (2000)
A.Morikawa、T.Yokochi 等人:“小鼠血管内皮细胞系中干扰素-γ 增强一氧化氮的产生及其通过肿瘤坏死因子-α 和脂多糖的调节。”Infect.Immun.. 68. 6209- 6214 (2000)
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10
    Role of tumor-suppressive genes on LPS-induced inflammatory response
    • 批准号:
      22590408
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.91万
    • 财政年份:
      2010
    • 负责人:
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    • 依托单位:
    Establishment of a new experimental model for human septic shock
    • 批准号:
      19590461
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $3.0万
    • 财政年份:
      2007
    • 负责人:
      YOKOCHI Takashi
    • 依托单位:
    The mechanism of the inhibitory action of lipopolysaccharide on anti-cancer drug-induced cell injury
    • 批准号:
      17590404
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.3万
    • 财政年份:
      2005
    • 负责人:
      YOKOCHI Takashi
    • 依托单位:
    Effect of activated protein C on LPS-induced nitric oxide production
    • 批准号:
      14570247
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.62万
    • 财政年份:
      2002
    • 负责人:
      YOKOCHI Takashi
    • 依托单位:
    海外基金