Inhaled hydrogen sulfide prevents neurodegeneration and movement disorder in a mouse model of Parkinson's disease

Kotaro Kida, Marina Yamada, Kentaro Tokuda, Eizo Marutani, Manabu Kakinohana, Masao Kaneki, Fumito Ichinose

研究成果: ジャーナルへの寄稿記事

97 引用 (Scopus)

抄録

Parkinson's disease is one of the major neurodegenerative disorders. Neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can cause Parkinson's disease-like symptoms and biochemical changes in humans and animals. Hydrogen sulfide (H2S) has been shown to protect neurons. The goal of this study was to examine the effects of inhaled H2S in a mouse model of Parkinson's disease induced by MPTP. Male C57BL/6J mice received MPTP at 80mg/kg and breathed air with or without 40 ppm H2S for 8h/day for 7 days. Administration of MPTP induced movement disorder and decreased tyrosine hydroxylase (TH)-containing neurons in the substantia nigra and striatum in mice that breathed air. Inhalation of H2S prevented the MPTP-induced movement disorder and the degeneration of TH-containing neurons. Inhaled H 2S also prevented apoptosis of the TH-containing neurons and gliosis in nigrostriatal region after administration of MPTP. The neuroprotective effect of inhaled H2S after MPTP administration was associated with upregulation of genes encoding antioxidant proteins, including heme oxygenase-1 and glutamate-cysteine ligase. These observations suggest that inhaled H 2S prevents neurodegeneration in a mouse model of Parkinson's disease induced by MPTP, potentially via upregulation of antioxidant defense mechanisms and inhibition of inflammation and apoptosis in the brain.

元の言語英語
ページ(範囲)343-352
ページ数10
ジャーナルAntioxidants and Redox Signaling
15
発行部数2
DOI
出版物ステータス出版済み - 7 15 2011
外部発表Yes

Fingerprint

Hydrogen Sulfide
Movement Disorders
Parkinson Disease
Neurons
Tyrosine 3-Monooxygenase
Up-Regulation
Antioxidants
Air
Apoptosis
Glutamate-Cysteine Ligase
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Heme Oxygenase-1
Gene encoding
Gliosis
Neurotoxins
Neuroprotective Agents
Substantia Nigra
4-phenyl-1,2,3,6-tetrahydropyridine
Inbred C57BL Mouse
Neurodegenerative Diseases

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

これを引用

Inhaled hydrogen sulfide prevents neurodegeneration and movement disorder in a mouse model of Parkinson's disease. / Kida, Kotaro; Yamada, Marina; Tokuda, Kentaro; Marutani, Eizo; Kakinohana, Manabu; Kaneki, Masao; Ichinose, Fumito.

:: Antioxidants and Redox Signaling, 巻 15, 番号 2, 15.07.2011, p. 343-352.

研究成果: ジャーナルへの寄稿記事

Kida, Kotaro ; Yamada, Marina ; Tokuda, Kentaro ; Marutani, Eizo ; Kakinohana, Manabu ; Kaneki, Masao ; Ichinose, Fumito. / Inhaled hydrogen sulfide prevents neurodegeneration and movement disorder in a mouse model of Parkinson's disease. :: Antioxidants and Redox Signaling. 2011 ; 巻 15, 番号 2. pp. 343-352.
@article{da5a7f87b3814f5298d38e2099021ede,
title = "Inhaled hydrogen sulfide prevents neurodegeneration and movement disorder in a mouse model of Parkinson's disease",
abstract = "Parkinson's disease is one of the major neurodegenerative disorders. Neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can cause Parkinson's disease-like symptoms and biochemical changes in humans and animals. Hydrogen sulfide (H2S) has been shown to protect neurons. The goal of this study was to examine the effects of inhaled H2S in a mouse model of Parkinson's disease induced by MPTP. Male C57BL/6J mice received MPTP at 80mg/kg and breathed air with or without 40 ppm H2S for 8h/day for 7 days. Administration of MPTP induced movement disorder and decreased tyrosine hydroxylase (TH)-containing neurons in the substantia nigra and striatum in mice that breathed air. Inhalation of H2S prevented the MPTP-induced movement disorder and the degeneration of TH-containing neurons. Inhaled H 2S also prevented apoptosis of the TH-containing neurons and gliosis in nigrostriatal region after administration of MPTP. The neuroprotective effect of inhaled H2S after MPTP administration was associated with upregulation of genes encoding antioxidant proteins, including heme oxygenase-1 and glutamate-cysteine ligase. These observations suggest that inhaled H 2S prevents neurodegeneration in a mouse model of Parkinson's disease induced by MPTP, potentially via upregulation of antioxidant defense mechanisms and inhibition of inflammation and apoptosis in the brain.",
author = "Kotaro Kida and Marina Yamada and Kentaro Tokuda and Eizo Marutani and Manabu Kakinohana and Masao Kaneki and Fumito Ichinose",
year = "2011",
month = "7",
day = "15",
doi = "10.1089/ars.2010.3671",
language = "English",
volume = "15",
pages = "343--352",
journal = "Antioxidants and Redox Signaling",
issn = "1523-0864",
publisher = "Mary Ann Liebert Inc.",
number = "2",

}

TY - JOUR

T1 - Inhaled hydrogen sulfide prevents neurodegeneration and movement disorder in a mouse model of Parkinson's disease

AU - Kida, Kotaro

AU - Yamada, Marina

AU - Tokuda, Kentaro

AU - Marutani, Eizo

AU - Kakinohana, Manabu

AU - Kaneki, Masao

AU - Ichinose, Fumito

PY - 2011/7/15

Y1 - 2011/7/15

N2 - Parkinson's disease is one of the major neurodegenerative disorders. Neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can cause Parkinson's disease-like symptoms and biochemical changes in humans and animals. Hydrogen sulfide (H2S) has been shown to protect neurons. The goal of this study was to examine the effects of inhaled H2S in a mouse model of Parkinson's disease induced by MPTP. Male C57BL/6J mice received MPTP at 80mg/kg and breathed air with or without 40 ppm H2S for 8h/day for 7 days. Administration of MPTP induced movement disorder and decreased tyrosine hydroxylase (TH)-containing neurons in the substantia nigra and striatum in mice that breathed air. Inhalation of H2S prevented the MPTP-induced movement disorder and the degeneration of TH-containing neurons. Inhaled H 2S also prevented apoptosis of the TH-containing neurons and gliosis in nigrostriatal region after administration of MPTP. The neuroprotective effect of inhaled H2S after MPTP administration was associated with upregulation of genes encoding antioxidant proteins, including heme oxygenase-1 and glutamate-cysteine ligase. These observations suggest that inhaled H 2S prevents neurodegeneration in a mouse model of Parkinson's disease induced by MPTP, potentially via upregulation of antioxidant defense mechanisms and inhibition of inflammation and apoptosis in the brain.

AB - Parkinson's disease is one of the major neurodegenerative disorders. Neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can cause Parkinson's disease-like symptoms and biochemical changes in humans and animals. Hydrogen sulfide (H2S) has been shown to protect neurons. The goal of this study was to examine the effects of inhaled H2S in a mouse model of Parkinson's disease induced by MPTP. Male C57BL/6J mice received MPTP at 80mg/kg and breathed air with or without 40 ppm H2S for 8h/day for 7 days. Administration of MPTP induced movement disorder and decreased tyrosine hydroxylase (TH)-containing neurons in the substantia nigra and striatum in mice that breathed air. Inhalation of H2S prevented the MPTP-induced movement disorder and the degeneration of TH-containing neurons. Inhaled H 2S also prevented apoptosis of the TH-containing neurons and gliosis in nigrostriatal region after administration of MPTP. The neuroprotective effect of inhaled H2S after MPTP administration was associated with upregulation of genes encoding antioxidant proteins, including heme oxygenase-1 and glutamate-cysteine ligase. These observations suggest that inhaled H 2S prevents neurodegeneration in a mouse model of Parkinson's disease induced by MPTP, potentially via upregulation of antioxidant defense mechanisms and inhibition of inflammation and apoptosis in the brain.

UR - http://www.scopus.com/inward/record.url?scp=79955667414&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79955667414&partnerID=8YFLogxK

U2 - 10.1089/ars.2010.3671

DO - 10.1089/ars.2010.3671

M3 - Article

VL - 15

SP - 343

EP - 352

JO - Antioxidants and Redox Signaling

JF - Antioxidants and Redox Signaling

SN - 1523-0864

IS - 2

ER -