Please use this identifier to cite or link to this item: http://ir.swu.ac.th/jspui/handle/123456789/14931
Title: 17β-Estradiol reduces nitrotyrosine immunoreactivity and increases SOD1 and SOD2 immunoreactivity in nigral neurons in male mice following MPTP insult
Authors: Tripanichkul W.
Sripanichkulchai K.
Duce J.A.
Finkelstein D.I.
Keywords: 1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine
3 nitrotyrosine
copper zinc superoxide dismutase
estradiol
manganese superoxide dismutase
1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine
3 nitrotyrosine
3-nitrotyrosine
biological marker
copper zinc superoxide dismutase
drug derivative
estradiol
manganese superoxide dismutase
neuroprotective agent
superoxide dismutase
tyrosine
unclassified drug
animal cell
animal experiment
article
cell count
controlled study
enzyme activation
female
glia cell
immunohistochemistry
immunoreactivity
male
mouse
nerve cell
neuroprotection
nonhuman
oxidative stress
priority journal
protein expression
substantia nigra
animal
C57BL mouse
drug effect
enzymology
glia
metabolism
nerve cell
oxidative stress
parkinsonism
pathophysiology
physiology
substantia nigra
upregulation
Animalia
Mus
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Animals
Biological Markers
Cell Count
Estradiol
Male
Mice
Mice, Inbred C57BL
Neuroglia
Neurons
Neuroprotective Agents
Oxidative Stress
Parkinsonian Disorders
Substantia Nigra
Superoxide Dismutase
Tyrosine
Up-Regulation
Issue Date: 2007
Abstract: Emerging evidence suggests the beneficial effects of estrogen on Parkinson's disease (PD), yet the mechanisms of action implicated remain elusive. While experimental evidence suggests that estrogen possesses potent antioxidative properties, it is still unknown whether the hormone exhibits a neuroprotection in a PD animal model through its antioxidant activities. This study therefore investigated the effects of 17β-estradiol (E2) on the immunoreactivity of nigral neurons and glia for nitrotyrosine (NT, a stable marker for oxidative stress), Cu/Zn superoxide dismutase (SOD1) and Mn superoxide dismutase (SOD2) in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model. Adult male mice were treated with E2 or vehicle for 11 days during which they were injected with MPTP or saline on the sixth day. The brains were collected on day 11 and quantitative immunohistochemistry was used to assess the number of NT-, SOD1- and SOD2-immunoreactive (IR) cells in the substantia nigra pars compacta (SNpc). In saline-treated group, E2 decreased NT-IR neuronal number and raised SOD1 and SOD2 expression in neurons and glia in the SNpc. MPTP induced a significant increase in the number of NT- and SOD2-IR neurons, but decreased the number of SOD1-IR neurons. MPTP also triggered a significant increase of SOD2- and SOD1-IR glial number. E2 pretreatment in MPTP mice reduced the number of NT-IR neurons, increased the number of SOD1- and SOD2-IR neurons, but did not alter the MPTP effect on glia immunoreactive to either SOD. Stimulation of SOD1 and SOD2 expression in nigral neurons suggests that E2 provides neuroprotection against MPTP-induced oxidative stress, partly through its ability to act as an antioxidant. © 2007 Elsevier B.V. All rights reserved.
URI: https://www.scopus.com/inward/record.uri?eid=2-s2.0-34547590252&doi=10.1016%2fj.brainres.2007.05.076&partnerID=40&md5=d3b4d9b37b2c9d75b18675f97ab841cc
http://ir.swu.ac.th/jspui/handle/123456789/14931
ISSN: 68993
Appears in Collections:Scopus 1983-2021

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