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Fundamental research of the effect of a variety of chemotherapeutics on leukocyte functions

Fundamental research of the effect of a variety of chemotherapeutics on leukocyte functions
多种化疗药物对白细胞功能影响的基础研究
批准号:
10671759
负责人:
OHURA Kiyoshi
金额:
$1.66万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1998
资助国家:
日本
项目状态:
已结题
起止时间:
1998 至 1999

项目摘要

项目成果

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相关文献

中文摘要
翻译
巨噬细胞和中性粒细胞在自然宿主防御系统中起重要作用。当这些吞噬细胞识别外来颗粒如细菌和真菌时,它们逃离血管系统,向感染部位迁移,随后通过来自超氧阴离子的杀菌活性氧物质吞噬和细胞内杀死入侵的微生物。为了确定抗菌药物是否影响这些功能,我们检测了6种新喹诺酮类药物,氧氟沙星(OFLX),洛美沙星(LFLX),托氟沙星(FLRX),氟罗沙星(FLRX),司帕沙星(SPFX)和左氧氟沙星(LVFX)对大鼠外周血巨噬细胞和中性粒细胞功能的影响。在体外治疗的新喹诺酮类药物是有效的显着增强超氧阴离子的产生在巨噬细胞。TFLX延长了超氧阴离子产生的增强作用,但OFLX、LFLX、FLRX、SPFX和LVFX是短暂的。与此相反,TFLX显著增强巨噬细胞的粘附, ...更多信息 年龄其他新喹诺酮类药物对巨噬细胞粘附无明显影响。此外,所有新喹诺酮类化合物均能显著抑制大肠杆菌的趋化和吞噬作用。巨噬细胞中的大肠杆菌。此外,OFLX、LFLX、TFLX和LVFX在显著增强巨噬细胞中过氧化氢的产生方面是有效的,而其他药剂对此没有影响。而OFLX、LFLX、FLRX和LVFX则能增强E.中性粒细胞中的大肠杆菌。然而,TFLX和SPFX未能显着影响中性粒细胞的吞噬作用。此外,LFLX和SPFX显着增强中性粒细胞的粘附。TFLX的增强作用与嗜中性粒细胞中超氧阴离子的产生有关,而其他五种新喹诺酮类药物可有效地显著减少嗜中性粒细胞中的超氧阴离子的产生。此外,TFLX是有效的显着增强中性粒细胞中过氧化氢的生产,而司帕沙星显着抑制这种生产。因此,新的喹诺酮类药物可能对巨噬细胞和中性粒细胞的功能产生不同的影响。少
英文摘要
Macrophages and neutrophils play an important role in natural host defense system. When these phagocytes recognize foreign particles, such as bacterium and fungi, they escape the vascular system, migrate towards the site of infection, followed by phagocytosis and intracellular killing of the invading microorganisms by bactericidal reactive oxygen species derived from the superoxide anion. To determine whether antimicrobials affect these functions, we examined the effect of 6 new quinolones, ofloxacin (OFLX), lomefloxacin (LFLX), tosufloxacin (FLRX), fleroxacin (FLRX), sparfloxacin (SPFX) and levofloxacin (LVFX) on the function of rat peripheral macrophages and neutrophils. In vitro treatment of the new quinolones was effective in markedly potentiating the production of superoxide anion in macrophages. The potentiation of the production of superoxide anion is prolonged with TFLX but transient for OFLX, LFLX, FLRX, SPFX and LVFX. In contrast, TFLX markedly potentiated adhesion in macroph … More ages. No significant alteration was detected in the adhesion in macrophages treated with the other new quinolones. In addition, all of the new quinolones significantly inhibited chemotaxis and phagocytosis of E. coli in macrophages. Moreover, OFLX, LFLX, TFLX, and LVFX were effective in significantly potentiating the production of hydrogen peroxide in macrophages, while the other agents did not affect that. By contrast, OFLX, LFLX, FLRX and LVFX caused an increase of phagocytosis of E. coli in neutrophils. However, TFLX and SPFX failed to significantly affect phagocytosis in neutrophils. Furthermore, LFLX and SPFX significantly potentiated adhesion of neutrophils. A potentiation by TFLX was seen with the production of superoxide anion in neutorphils, while the other five new quinolones were effective in markedly reducing that production in neutrophils. Moreover, TFLX was effective in significantly potentiating the production of hydrogen peroxide in neutrophils, whereas sparfloxacin markedly inhibited such production. Therefore, the new quinolones may differentially affect the function of macrophages and neutrophils. Less
期刊论文(5)
专著(0)
科研奖励(0)
会议论文
東 泰孝: "ニューキノロン薬のマクロファージ機能に及ぼす影響" 日本薬理学雑誌. 113(3). 48P (1999)
Yasutaka Azuma:“新喹诺酮类药物对巨噬细胞功能的影响”日本药理学杂志 113(3) 48P (1999)。
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通讯作者:
Azuma Y, Shinohara M and Ohura K: "Effect of new quinolones on macrophage functions"Folia pharmacologica japonica. 113(3). 48 (1999)
Azuma Y、Shinohara M 和 Ohura K:“新型喹诺酮类药物对巨噬细胞功能的影响”Folia drugologica japonica。
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通讯作者:
Yasutaka Azuma: "Interaction between new quinolones and fuctions of macrophages" Journal of Dental Research. 78(Special Issue). 183 (1999)
Yasutaka Azuma:“新喹诺酮类药物与巨噬细胞功能之间的相互作用”牙科研究杂志。
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通讯作者:
Azuma Y, Shinohara M and Ohura K: "Possible interaction of new quinolones with phagocytes."Current Topics in Pharmacology. (in press). (2000)
Azuma Y、Shinohara M 和 Ohura K:“新喹诺酮类药物与吞噬细胞的可能相互作用。”药理学当前主题。
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通讯作者:
Differentiation of the expression of adenosine receptor affect LPS-induced cytokine production by leukocytes
  • 批准号:
    19592164
  • 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:
    OHURA Kiyoshi
  • 依托单位:
Comparative studies of the effect of adenosine and ATP affect LPS induced inflammation
  • 批准号:
    15591987
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.24万
  • 财政年份:
    2003
  • 负责人:
    OHURA Kiyoshi
  • 依托单位:
Crosstalk between transcription factors responsive to LPS and anti-inflammatory agents
  • 批准号:
    13671957
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $1.92万
  • 财政年份:
    2001
  • 负责人:
    OHURA Kiyoshi
  • 依托单位:
Studies on leukocyte function of periodontal desease and diabetes mellitus
  • 批准号:
    06671896
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
  • 资助金额:
    $1.22万
  • 财政年份:
    1994
  • 负责人:
    OHURA Kiyoshi
  • 依托单位:
国内基金
海外基金
上皮祖细胞应答巨噬细胞分泌因子IL-1β参与炎症微环境下输卵管纤毛分化障碍的机制研究
  • 批准号:
    82371691
  • 项目类别:
    面上项目
  • 资助金额:
    49.00万元
  • 批准年份:
    2023
  • 负责人:
    张健
  • 依托单位:
LIPUS促进微环境巨噬细胞释放CCL2诱导尿道周围平滑肌祖细胞定植与分化的机制研究
  • 批准号:
    82370780
  • 项目类别:
    面上项目
  • 资助金额:
    49.00万元
  • 批准年份:
    2023
  • 负责人:
    夏术阶
  • 依托单位:
SENP1调控巨噬细胞极性参与老年心肌纤维化的作用及机制
  • 批准号:
    82371584
  • 项目类别:
    面上项目
  • 资助金额:
    49.00万元
  • 批准年份:
    2023
  • 负责人:
    薛松
  • 依托单位:
RAI16负调控肿瘤相关巨噬细胞c/EBPβ-TGF-β1通路抑制结直肠癌的机制研究
  • 批准号:
    32100629
  • 项目类别:
    青年科学基金项目(C类)
  • 资助金额:
    30.0万元
  • 批准年份:
    2021
  • 负责人:
    丁翠玲
  • 依托单位: