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

Research output: Contribution to journalArticlepeer-review

107 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)343-352
Number of pages10
JournalAntioxidants and Redox Signaling
Volume15
Issue number2
DOIs
Publication statusPublished - Jul 15 2011
Externally publishedYes

All Science Journal Classification (ASJC) codes

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

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