Effect of Hypoxia Mimetic Cobalt Chloride on the Expression of Extracellular-Superoxide Dismutase in Retinal Pericytes
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- Adachi Tetsuo
- Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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- Aida Kazunari
- Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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- Nishihara Hiroko
- Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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- Kamiya Tetsuro
- Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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- Hara Hirokazu
- Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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The initial clinical stage of diabetic retinopathy (DR) is characterized by the development of intraretinal microvascular abnormalities. The increased formation of reactive oxygen species (ROS) is thought to be a key event in the pathogenesis of DR. Extracellular-superoxide dismutase (EC-SOD) is an anti-inflammatory enzyme that is distributed mainly in vascular cells and protects cells from ROS by scavenging superoxide anion. Treatment with cobalt chloride (CoCl2) decreased the expression of EC-SOD but not other SOD isozymes in pericytes accompanied with an increase of intracellular ROS production. Pre-treatment with N-acetylcysteine (NAC) significantly suppressed the ROS production and down-regulation of EC-SOD. We observed the activation of caspase-3 and DNA fragmentation as signs of apoptotic process by CoCl2 treatment. In addition, these phenomena were significantly inhibited by pre-treatment with NAC. EC-SOD enhancer 4-phenyl butyric acid also suppressed the caspase-3 activation. It is known that the presence of a high level of EC-SOD throughout the vessel walls might have an important protective role against superoxide in the vascular system. The decrease in EC-SOD expression accompanied with elevation of ROS level in pericytes under hypoxia might induce and/or promote the ROS-triggered apoptosis of pericytes and the development of pathogenesis in DR.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 34 (8), 1297-1300, 2011
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204632739584
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- NII論文ID
- 130000936602
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC3Mjis1WjtA%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 11174801
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- PubMed
- 21804221
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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- PubMed
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