Cyclo-oxygenase-2 deficient mice are less susceptible to MPTP than wild-type mice

Z Feng, D Li, PCW Fung, Z Peia, David Ramsden, Y Han, S-L Ho

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63 Citations (Scopus)


The primary lesion in Parkinson's disease is the death of dopaminergic neurons in the substantia nigra. The role of cyclooxygenase (COX)-2 in the etiology of Parkinson's disease was explored using COX-2 gene knockout mice. Mortality after injection of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP, a chemical known to cause parkinsonism in humans) in heterozygous COX-2-deficient mice was lower than that in wild-type mice. The number of tyrosine hydroxylase immunoreactive neurons in the substantia nigra pars compacta of MPTP-treated wild-type mice declined to a greater extent than in heterozygous mice. Inhibition of COX-2 protein expression decreased the lesion caused by MPTP and protected the dopaminergic neurons in substantia nigra pars compacta. This result suggested that inhibition of COX-2 has potential therapeutic implications.
Original languageEnglish
Pages (from-to)1927-1929
Number of pages3
Publication statusPublished - 1 Jan 2003


  • knockout mouse
  • MPTP
  • Parkinson's disease
  • COX-2
  • tyrosine hydroxylase
  • substantia nigra


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