Danthron Inhibits the Neurotoxicity Induced by Various Compounds Causing Oxidative Damages Including β-Amyloid (25-35) in Primary Cortical Cultures (Toxicology)

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概要

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• Oxidative stress caused by an elevation in reactive oxygen species (ROS) plays an important role in Alzheimer's disease and other neurodegenerative diseases. In this study, we examined the neuroprotective effect of danthron (1,8-dihydroxyanthraquinone) against neurotoxicities induced by β-amyloid (25-35), excitotoxins, apoptosis, and oxidative stress in primary cortical cultures. Danthron dose-dependently reduced neuronal injury induced by 30 μM β-amyloid (25-35). Danthron significantly inhibited oxidative injury induced by 100μM Fe^<3+> and decreased membrane lipid peroxidation induced by 100 μM Fe^<3+> as measured by thiobarbituric-acid-reactive substance (TBARS). Danthron (0.5-50 μM) ameliorated the effects of buthionine sulfoximine (BSO, 1 mM), which depletes endogenous glutathione by 10-73%. Danthron also dose-dependently inhibited neuronal injury mediated by nitric oxide (NO) radicals, but failed to inhibit injury due to superoxide radicals (O^<2->). These results suggest danthron treatment may, in part, reduce neurotoxicity related to β-amyloid protein by both dominant inhibitory effects on membrane lipid peroxidation and glutathione deprivation.

• 社団法人日本薬学会の論文
• 2004-05-01

著者

• KIM Hyoung-Chun

  Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University

• SONG Dong-Keun

  Department of Pharmacology, Hallym University College of Medicine, Institute of Natural Medicine

• Song Dong-keun

  Department Of Pharmacology And Institute Of Natural Medicine College Of Medicine Hallym University

• KWON Yong-Soo

  Neurotoxicology Program, Department of Pharmacy, College of Pharmacy, Kangwon National University

• KOH Jac-Young

  National Creative Research Initiative Center for the Study of CNS Zinc and Department of Neurology,

• KWON Myung-Sang

  Department of Veterinary Medicine, College of animal Resources Science, Kangwon National University

• CHOI Yeon-Sik

  Safety Evaluation Laboratory, Yuhan Research Institute

• WIE Myung-Bok

  Department of Veterinary Medicine, College of animal Resources Science, Kangwon National University

• Kim Hyoung-chun

  Neurotoxicology Program Coll. Of Pharmacy Korea Inst. Of Drug Abuse Kangwon National Univ.

• Kim H‐c

  Neurotoxicology Program Department Of Pharmacy College Of Pharmacy Kangwon National University

• Koh Jac-young

  National Creative Research Initiative Center For The Study Of Cns Zinc And Department Of Neurology C

• Wie Myung-bok

  Department Of Veterinary Medicine College Of Animal Resources Science Kangwon National University

• Kwon Yong-soo

  Neurotoxicology Program Department Of Pharmacy College Of Pharmacy Kangwon National University

• Choi Yeon-sik

  Safety Evaluation Laboratory Yuhan Research Institute

• Kim Hyoung-chun

  Neuropsychopharmacology And Toxicology Program Coll. Of Pharmacy Kangwon National Univ.

• Kwon Myung-sang

  Department Of Veterinary Medicine College Of Animal Resources Science Kangwon National University

• Koh Jae-Young

  National Creative Research Initiative Center for the Study of CNS Zinc and Department of Neurology, College of Medicine, Ulsan University

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