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HMG-CoA Reductase Inhibitors Suppress High Glucose-induced Excessive O2⁻ production in J-774 Cells
https://dmu.repo.nii.ac.jp/records/113
https://dmu.repo.nii.ac.jp/records/11373dc2cd2-4508-415f-900d-687142e8c876
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
KJ00000010444.pdf (908.9 kB)
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| Item type | [ELS]学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-05-24 | |||||
| タイトル | ||||||
| タイトル | HMG-CoA Reductase Inhibitors Suppress High Glucose-induced Excessive O2⁻ production in J-774 Cells | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | HMG-CoA inhibitors | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | superoxide anion | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | macrophage | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | high glucose | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 雑誌書誌ID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00629581 | |||||
| 論文名よみ | ||||||
| タイトル | HMG-CoA Reductase Inhibitors Suppress High Glucose-induced Excessive O2⁻ production in J-774 Cells | |||||
| 著者 |
Kawagoe, Yoshiaki
× Kawagoe, Yoshiaki× Kato, Tetsuya× Kase, Hiroyuki× Suzuki, Manabu× Sato, Noriyuki |
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| 著者所属(英) | ||||||
| 言語 | en | |||||
| 値 | Department of Endocrinology and Metabolism, Dokkyo University School of Medicine | |||||
| 著者所属(英) | ||||||
| 言語 | en | |||||
| 値 | Department of Endocrinology and Metabolism, Dokkyo University School of Medicine | |||||
| 著者所属(英) | ||||||
| 言語 | en | |||||
| 値 | Department of Endocrinology and Metabolism, Dokkyo University School of Medicine | |||||
| 著者所属(英) | ||||||
| 言語 | en | |||||
| 値 | Department of Endocrinology and Metabolism, Dokkyo University School of Medicine | |||||
| 著者所属(英) | ||||||
| 言語 | en | |||||
| 値 | Department of Endocrinology and Metabolism, Dokkyo University School of Medicine | |||||
| 記事種別(英) | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Original | |||||
| 抄録(英) | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Statins (HMG-CoA reductase inhibitors) have so-called pleiotropic effects, which directly reduce neoinitial inflammation of atherosclerosis, and one possible mechanism is the attenuation of oxidative stress. Although an increase in oxidant stress is suggested to cause and aggravate arteriosclerosis in diabetes, the origin of oxidant stress and effects of statins on the oxidant stress in diabetes are not clearly delineated. We evaluated in this study the effect of high glucose on superoxide anion (O_2^-) production in the J-774 macrophage-like cell line, and the effect of various statins (cerivastatin, fluvastatin, and nisvastatin) on it. The basal and 12-O-tetradecanoylphor-bol 13-acetate (TPA)-stimulated O_2^- productions were measured by chemiluminescence (CL) amplified with a Cypridina luciferin analog. Both basal CL and TPA-stimulated CL (TPA-CL) in J-774 cells cultured with high glucose were apparently increased in dose and time dependent manners, and the increments were clearly suppressed by a NADPH oxidase inhibitor (diphenyleneiodonium chloride) or a protein kinase C inhibitor (GF-109803 X). Three statins significantly inhibited the high glucose-induced excessive O_2^- production in a dose dependent manner. Furthermore, co-incubation with mevalonic acid and the metabolites, geranylgeranyl pyrophosphate and farnesyl pyrophosphate, partially prevented the statin-induced suppression of TPA-CL. These data suggest that in J-774 cells high glucose causes excessive O_2^- production through NADPH oxidase and protein kinase C pathways, and statins suppress the excessive O_2^- generation. This effect of statins could be, in part, dependent on the inhibition of synthesis of isoprenoid intermediates. Statins may be useful as a drug to prevent arteriosclerosis by inhibiting oxidative stress in poorly controlled diabetic patients. | |||||
| 書誌情報 |
Dokkyo journal of medical sciences 巻 30, 号 1, p. 13-21, 発行日 2003-03-25 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 03855023 | |||||
