The effect of perioperatively used drugs on the HIF-1 activation and its downstream gene expressions.

围手术期使用药物对HIF-1激活及其下游基因表达的影响。

基本信息

  • 批准号:
    15390481
  • 负责人:
  • 金额:
    $ 9.09万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 财政年份:
    2003
  • 资助国家:
    日本
  • 起止时间:
    2003 至 2005
  • 项目状态:
    已结题

项目摘要

Hypoxia (reduced oxygen availability) induces a series of adaptive physiological responses. At the cellular level, the adaptation includes a switch of energy metabolism from oxidative phosphorylation to anaerobic glycolysis, increased glucose uptake, and the expression of stress proteins related to cell survival One of the most important transcription factors that activate the expression of oxygen-regulated genes is hypoxia-inducible factor 1 (HIF-1). In this study, we investigated the effect of perioperatively used drugs including anesthetics, vasodilators, and analgesics on the HIF-1 activation and its downstream gene expressions.Results are as followings.1.The intravenous anesthetic propofol reversibly inhibits HIF-1 activity and the gene expression mediated by HIF-1 by blocking the synthesis of the HIF-1α subunit under 20 or 5% O_2 conditions, but not under 1% O_2 conditions. In contrast, thyamylal and thiopental blocks HIF-1 activation under 1% O_2 conditions.2.The local anesthetics lidocaine or bupivacaine does not affect the HIF-1-dependent cellular hypoxia-induced gene responses.3.Either of DAGO, DPDPE, and U-50488, which are the selective agonists of μ-, κ-, and δ-opioid receptors, respectively did not affect the HIF-1 activation by hypoxia. The selective agonists of opioid receptors do not affect the HIF-1-dependent cellular hypoxia-induced gene responses.4.We demonstrate that among the three nitrates, only SNP inhibits HIF-1 activation in response to hypoxia. In contrast, NTG or ISDN does not affect HIF-1 activity. SNP inhibits the accumulation of HIF-1α, the regulatory subunit of HIF-1, and the transcriptional activation of HIF-1α via a mechanism that is not dependent on either NO or soluble guanylate cyclase.
缺氧(氧可用性降低)诱导一系列适应性生理反应。在细胞水平上,这种适应包括能量代谢从氧化磷酸化转换为无氧糖酵解,增加葡萄糖摄取,以及与细胞存活相关的应激蛋白的表达。激活氧调节基因表达的最重要的转录因子之一是缺氧诱导因子1(HIF-1)。本研究探讨了围手术期使用的麻醉药、扩血管药和镇痛药对缺氧诱导因子-1(HIF-1)活性及其下游基因表达的影响,结果如下:1.静脉麻醉药异丙酚在20或5%O_2条件下,通过阻断HIF-1α亚基的合成,可逆性地抑制HIF-1活性及其下游基因表达;而在1%O_2条件下则没有。局部麻醉药利多卡因和布比卡因不影响低氧诱导的HIF-1依赖性细胞基因反应; μ-、κ-和δ-阿片受体选择性激动剂DAGO、DPDPE和U-50488均不影响低氧诱导的HIF-1激活。选择性阿片受体激动剂不影响HIF-1依赖的细胞缺氧诱导的基因反应。4.我们证明了在三种硝酸盐中,只有SNP抑制HIF-1对缺氧的反应。相反,NTG或ISDN不影响HIF-1活性。SNP通过一种不依赖于NO或可溶性鸟苷酸环化酶的机制抑制HIF-1α(HIF-1 α的调节亚基)的积累和HIF-1α的转录激活。

项目成果

期刊论文数量(28)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Induction of hypoxia-inducible factor 1 activity by muscarinic acetylcholine receptor signaling
  • DOI:
    10.1074/jbc.m405164200
  • 发表时间:
    2004-10-01
  • 期刊:
  • 影响因子:
    4.8
  • 作者:
    Hirota, K;Fukuda, R;Semenza, GL
  • 通讯作者:
    Semenza, GL
Kerry, B., Hackett, SF, 他: "Cell-Type-Specific Regulation of Angiogenic Growth Factor Gene Expression and Induction of Angiogenesis in Non-Ischemic Tissue by a Constitutively-Active Form of Hypoxia-Inducible Factor 1"Circulation Research. 93. 1074-1081 (2
Kerry, B.、Hackett, SF 等人:“细胞类型特异性调节血管生成生长因子基因表达和通过缺氧诱导因子 1 的组成型活性形式诱导非缺血组织中的血管生成”循环研究93.1074-1081 (2
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Induction of hypoxia-inducible factor 1 activity by muscarinic acetylcholine receptor signalling.
通过毒蕈碱乙酰胆碱受体信号传导诱导缺氧诱导因子 1 活性。
  • DOI:
  • 发表时间:
    2004
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Hirota;K.
  • 通讯作者:
    K.
Activation of hypoxia-inducible factor 1 during macrophage differentiation
Opioid receptor stimulation does not affect cellular hypoxia-induced gene responses mediated by hypoxia-inducible factor 1 in cultured cell lines.
阿片受体刺激不会影响培养细胞系中缺氧诱导因子 1 介导的细胞缺氧诱导的基因反应。
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Takabuchi;S.;Hirota;K,.Oda;S.;Nish;K.;Oda;T.;Shingu;K.;Adachi;T.;Fukuda K.
  • 通讯作者:
    Fukuda K.
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ADACHI Takehiko其他文献

ADACHI Takehiko的其他文献

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{{ truncateString('ADACHI Takehiko', 18)}}的其他基金

The role of cellular redox system in inflammatory disorders of acute lung injury
细胞氧化还原系统在急性肺损伤炎症性疾病中的作用
  • 批准号:
    15K10551
  • 财政年份:
    2015
  • 资助金额:
    $ 9.09万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Cell biological analysis of the effect of hypoxia-induced gene expressions on progression of pulmonary alveolar inflammation
缺氧诱导基因表达对肺泡炎症进展影响的细胞生物学分析
  • 批准号:
    21591992
  • 财政年份:
    2009
  • 资助金额:
    $ 9.09万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Cellular and molecular biological analysis of hypoxia-inducible genetic responses in lung epithelial cells
肺上皮细胞缺氧诱导遗传反应的细胞和分子生物学分析
  • 批准号:
    19591827
  • 财政年份:
    2007
  • 资助金额:
    $ 9.09万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Electrophysiological study on the antinociceptive effect of xenon.
氙抗伤害作用的电生理学研究。
  • 批准号:
    10671411
  • 财政年份:
    1998
  • 资助金额:
    $ 9.09万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
The effect of inhalation anesthetic on wind up phenomenon of spinal dorsal horn neurons
吸入麻醉药对脊髓背角神经元缠绕现象的影响
  • 批准号:
    08671733
  • 财政年份:
    1996
  • 资助金额:
    $ 9.09万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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围术期中性粒细胞胞外陷阱表达分析
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麻醉及围手术期自动给药控制系统的研究
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以水通道蛋白为重点的新型围手术期输注控制策略的制定
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围手术期远程预康复系统的开发及有效性验证
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