Antioxidative Potential of Fluvastatin via the Inhibition of Nicotinamide Adenine Dinucleotide Phosphate (NADPH) Oxidase Activity
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概要
- 論文の詳細を見る
We previously reported that fluvastatin, a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, a strong lipid lowering drug, exerted an anti-atherosclerotic effect at doses insufficient to lower serum lipids in cholesterol fed rabbits. The evidence demonstrated that the superoxide anions from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a critical role in several steps in the development of atherosclerosis. This study was designed to determine the effects of HMG-CoA reductase inhibitors on the production of the superoxide anions of NADPH oxidase in isolated rat peritoneal neutrophils. Fluvastatin (1-10μM) decreased phorbol 12-myristate 13-acetate (PMA, 10nM)-dependent reactive oxygen species (ROS) generation in a concentration-dependent manner. It also (10μM) decreased PMA-dependent O_2, consumption of the rat neutrophils. These effects were reversed by the addition of mevalonate, a metabolite in the HMG-CoA reductase pathway. Treatment with pravastatin did not show any significant changes. Fluvastatin (10μM) decreased ROS, such as hydroxyl radicals and superoxide anions generated by the Fenton reaction, and by the xanthine-xanthine oxidase system. Rats were treated with either fluvastatin (5 mg/kg per day, p.o.) or pravastatin (5 mg/kg per day, P.O.) for 1 week. Treatment with fluvastatin decreased the PMA-dependent ROS generation. The fluvastatin induced effect on the PMA-dependent ROS generation was reversed by the combined administration with 40 mg/kg mevalonate per day. The antioxidative effect of fluvastatin was thought to have caused not only the scavenging action of the radicals but also to have inhibited ROS generation by inhibiting the NADPH oxidase activity. This antioxidative potential of fluvastatin via the inhibition of NADPH oxidase activity may be profitable in preventing atherosclerosis.
- 公益社団法人日本薬学会の論文
- 2003-06-01
著者
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INOUE Masayasu
Department of Biochemistry I, Osaka City University Medical School
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Hoshi K
Laboratory Of Pharmacotherapeutics Showa Pharmaceutical University
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Sato Eisuke
Department of Biochemistry Osaka City University Medical School
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NAKASHIMA Akinori
Department of Biology, Faculty of Science, Kagoshima University
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Inoue M
Nagoya‐city Univ. Aichi Jpn
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Inoue Masayasu
Department Of Biochemistry & Molecular Pathology Osaka City University Medical School
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Hoshi Katsuji
Laboratory Of Pharmacotherapeutics Showa Pharmaceutical University
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BANDOH Tsutomu
Department of Clinical Pharmacology, Hokkaido College of Pharmacy
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MITANI Hironobu
Department of Pharmacology, Novartis Tsukuba Research Institute
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HOSHI Katsuji
Department of Clinical Pharmacology, Hokkaido College of Pharmacy
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Nakashima Akinori
Department Of Pharmacology Novartis Tsukuba Research Institute
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Nakashima Akinori
Department Of Biology Faculty Of Science Kagoshima University
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Sato Eisuke
Department Of Biochemistry And Molecular Pathology. Osaka City University Medical School
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Sato Eisuke
Department Of Biochemistry And Molecular Pathology
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Hoshi Katsuji
Department Of Clinical Pharmacology Hokkaido College Of Pharmacy
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Bandoh Tsutomu
Department Of Clinical Pharmacology Hokkaido College Of Pharmacy
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Mitani Hironobu
Department Of Pharmacology Novartis Tsukuba Research Institute
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SATO Eisuke
Department of Applied Molecular Bioscience, Graduate School of Medicine, Yamaguchi University
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