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演題詳細

Poster

パーキンソン病とその類縁疾患
Parkinson's Disease and Related Disorders

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

分子状水素による胃‐脳連関とパーキンソン病モデル動物
Stomach-brain interaction induced by molecular hydrogen in Parkinson's disease model animal

  • P3-291
  • 井上 太海 / Taikai Inoue:1 松本 明郎 / Akio Matsumoto:2,3,5 山藤 芽実 / Megumi Yamafuji:1 立花 知子 / Tomoko Tachibana:2 中谷 晴昭 / Haruaki Nakaya:2 中別府 雄作 / Yusaku Nakabeppu:4,5 野田 百美 / Mami Noda:1,5 
  • 1:九州大学 薬学部・薬学府  医療薬科学専攻 生命薬学講座 病態生理学分野 / Laboratory of Pathophysiology, Faculty of Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, School of Pharmaceutical Sciences, Kyushu University 2:千葉大学大学院医学研究院薬理学 / Department of Pharmacology, Graduate School of Medicine, Chiba University, Chiba 3:九州大学生体防御医学研究所 防御分子構築学分野 / Division of Molecular Design, Medical Institute of Bioregulation, Kyushu University, Fukuoka 4:九州大学生体防御医学研究所 脳機能制御学分野 / Division of Neurofunctional Genomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka 5:国立大学法人 九州大学 ヌクレオチドプール研究センター / Research Center for Nucleotide Pool, Kyushu University, Fukuoka, Japan 

Parkinson's disease (PD) has been a major focus in the field of oxidative stress and disease, because it is thought that degeneration of dopaminergic neurons can be triggered and aggravated by the accumulation of oxidative damage. We have previously showed that H2 in drinking water reduced dopaminergic neuronal loss in MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-induced PD model mice. However, inhalation of H2 did not remain in brain tissue for several minutes and drinking water with saturated H2 (hydrogen water) did not increase H2 concentration in striatum. These results may imply that the effect of H2 is an indirect effect. Here we show that H2 supplementation increases gastric expression of mRNA encoding ghrelin, a growth hormone secretagogue, and ghrelin secretion, which are antagonized by the β1-adrenoceptor blocker, atenolol. Strikingly, the neuroprotective effect of H2 water was abolished by either administration of the ghrelin receptor-antagonist, D-Lys3 GHRP-6, or atenolol. Thus, the neuroprotective effect of H2 water in PD is mediated by enhanced production of ghrelin. Our findings point to potential, novel strategies for ameliorating pathophysiology in which a protective effect of H2 supplementation has been demonstrated. In addition, a contribution of ghrelin via parasympathetic is discussed.

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