<Original Paper>HMG-CoA Reductase Inhibitors Suppress High Glucose-induced Excessive O_2^- production in J-774 Cells
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概要
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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.
- 獨協医科大学の論文
- 2003-03-25
著者
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KATO Tetsuya
Department of Physics,Faculty of Science,Tokyo Institute of Technology
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Sato N
Department Of Orthopedic Surgery Sapporo Medical University School Of Medicine
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Sato Noriyuki
Department Of Orthopedic Surgery Sapporo Medical University School Of Medicine
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Sato N
Department Of Pathology Sapporo Medical University School Of Medicine
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Suzuki Manabu
Department Of Endocrinology And Metabolism Dokkyo University School Of Medicine
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Kase Hiroyuki
Dokkyo Univ. School Of Medicine Tochigi Jpn
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Kase Hiroyuki
Department Of Astronomy School Of Science The University Of Tokyo
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Kase Hiroyuki
Department Of Endocrinology & Metabolism Dokkyo University School Of Medicine
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Kawagoe Yoshiaki
Department Of Endocrinology And Metabolism Dokkyo University School Of Medicine
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Kato Tetsuya
Department Of Information Science And Engineering Shibaura Institute Of Technology
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Kato T
Department Of Endocrinology And Metabolism Dokkyo University School Of Medicine
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Sato Noriyuki
Department Of Biological Chemistry Faculty Of Agriculture Yamaguchi University
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Sato Noriyuki
Department of Endocrinology and Metabolism, Dokkyo University School of Medicine
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Kase Hiroyuki
Department of Endocrinology and Metabolism, Dokkyo University School of Medicine
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Kato Tetsuya
Department of Endocrinology and Metabolism, Dokkyo University School of Medicine
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Kawagoe Yoshiaki
Department of Endocrinology & Metabolism, Dokkyo Medical University, Japan
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