Indomethacin Ameliorates Trimethyltin-Induced Neuronal Damage <i>in Vivo</i> by Attenuating Oxidative Stress in the Dentate Gyrus of Mice
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- Huong Nguyen Quynh
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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- Nakamura Yukary
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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- Kuramoto Nobuyuki
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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- Yoneyama Masanori
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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- Nagashima Reiko
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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- Shiba Tatsuo
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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- Yamaguchi Taro
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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- Hasebe Shigeru
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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- Ogita Kiyokazu
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
Bibliographic Information
- Other Title
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- Highlighted paper selected by Editor-in-Chief : Indomethacin Ameliorates Trimethyltin-Induced Neuronal Damage in Vivo by Attenuating Oxidative Stress in the Dentate Gyrus of Mice
- Indomethacin ameliorates trimethyltin-induced neuronal damage <italic>in vivo</italic> by attenuating oxidative stress in the dentate gyrus of mice
- Indomethacin ameliorates trimethyltin-induced neuronal damage in vivo by attenuating oxidative stress in the dentate gyrus of mice
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Abstract
The organotin trimethyltin (TMT) is well known to cause neuronal degeneration in the hippocampal dentate gyrus of mice. The first purpose of the present study was to examine whether the cyclooxygenase (COX) inhibitor indomethacin could ameliorate neuronal degeneration in the dentate gyrus of mice following TMT treatment in vivo. The systemic injection into mice of TMT at 2.8 mg/kg produced activation of endogenous caspase-3 and calpain, enhanced the gene expression of COX-1 and COX-2, activated microglial cells, and caused the formation of the lipid peroxidation product 4-hydroxynonenal in the hippocampus. Given at 12-h post-TMT treatment, the systemic injection of indomethacin (5 or 10 mg/kg, subcutaneously) significantly decreased the TMT-induced damage to neurons having active caspase-3 and single-stranded DNA in the dentate granule cell layer of the hippocampus. The results of the α-Fodrin degradation test revealed that the post-treatment with indomethacin was effective in attenuating TMT-induced activation of endogenous caspases and calpain in the hippocampus. In TMT-treated animals, interestingly, the post-treatment with indomethacin produced not only activation of microglial cells in the dentate gyrus but also the formation of 4-hydroxynonenal in the dentate granule cell layer. Taken together, our data suggest that COX inhibition by indomethacin ameliorated TMT-induced neuronal degeneration in the dentate gyrus by attenuating intensive oxidative stress.
Journal
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- Biological and Pharmaceutical Bulletin
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Biological and Pharmaceutical Bulletin 34 (12), 1856-1863, 2011
The Pharmaceutical Society of Japan
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Details 詳細情報について
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- CRID
- 1390001204632407040
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- NII Article ID
- 130001872607
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- NII Book ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC38%2FjvVygtw%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL BIB ID
- 023321606
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- PubMed
- 22130242
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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