Effect of Nitric Oxide on .BETA.-Glucan/Indomethacin-Induced Septic Shock
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- Nameda Sachiko
- Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
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- Saito Maki
- Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
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- Miura Noriko N.
- Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
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- Adachi Yoshiyuki
- Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
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- Ohno Naohito
- Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
Bibliographic Information
- Other Title
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- Effect of Nitric Oxide on β-Glucan/Indomethacin-Induced Septic Shock
- Effect of Nitric Oxide on ベータ Glucan Indomethacin Induced Septic Shock
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Abstract
We have previously shown that repeated administration of nonsteroidal anti-inflammatory drugs (NSAIDs) to mice treated with β-glucan, a biological response modifier, induced severe lethality. The lethality would be strongly related to the translocation of enterobacterial flora to the peritoneal cavity and disruption of the cytokine network. Reports suggest that nitric oxide (NO) can have an effective or detrimental role in septic shock. In the present study, we examined the effect of NO, an inflammatory mediator, on β-glucan/indomethacin (IND)- induced septic shock by inhibiting its synthesis with NG-nitro-L-arginine methyl ester (L-NAME), a nonselective NO synthase (NOS) inhibitor. Nitrite concentration was used as an indicator of NO generation. Mortality in β-glucan/IND-treated mice was increased by administering L-NAME. Numbers of bacteria in various organs of mice treated with β-glucan/IND rose significantly within a couple of days of the administration of L-NAME. Additionally, TNF-α, IL-1β, and IL-6 concentrations were enhanced in peritoneal exuded cells in culture. These results suggest a significant loss of the bactericidal activity of macrophages on the administration of a NOS inhibitor which enhanced the rate of enterobacterial invasion to the peritoneal cavity, resulting in systemic inflammatory response syndrome. The production of NO, therefore, provides a protective effect in β-glucan/IND-induced sepsis.
Journal
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- Biological and Pharmaceutical Bulletin
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Biological and Pharmaceutical Bulletin 28 (7), 1254-1258, 2005
The Pharmaceutical Society of Japan
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Keywords
Details 詳細情報について
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- CRID
- 1390282679604952832
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- NII Article ID
- 10016665495
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- NII Book ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL BIB ID
- 7343587
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- PubMed
- 15997109
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- Abstract License Flag
- Disallowed