Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/15030
Title: Estrogen down-regulates glial activation in male mice following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine intoxication
Authors: Tripanichkul W.
Sripanichkulchai K.
Finkelstein D.I.
Keywords: 1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine
estradiol
estrogen
tyrosine 3 monooxygenase
animal cell
animal model
animal tissue
article
astrocyte
cell activation
cell loss
controlled study
corpus striatum
disease model
down regulation
glia cell
immunocompetent cell
immunohistochemistry
injection
male
mouse
nerve cell
nerve fiber
neuroprotection
nonhuman
Parkinson disease
priority journal
quantitative analysis
substantia nigra
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Analysis of Variance
Animals
Basal Ganglia
Cell Count
Cell Death
Disease Models, Animal
Drug Administration Schedule
Estrogens
Gene Expression Regulation
Glial Fibrillary Acidic Protein
Immunohistochemistry
Lectins
Male
Mice
Mice, Inbred C57BL
Neuroglia
Neurons
Neurotoxicity Syndromes
Tyrosine 3-Monooxygenase
Animalia
Issue Date: 2006
Abstract: Emerging evidence suggests beneficial effect of estrogen for Parkinson's disease (PD), yet the exact mechanisms implicated remain obscured. Activated glia observed in MPTP mouse model and in PD may participate in the cascade of deleterious events that ultimately leads to dopaminergic nigral neuronal death. In vitro studies demonstrate that estrogen can modify the microglial and astroglial expression of inflammatory mediator, such as cytokines and chemokines implicated in neuroinflammation and neurodegeneration. To determine whether estrogen-elicited neuroprotection in PD is mediated through glia, adult male C57Bl/6 mice were treated with 17β-estradiol (E2) for a total of 11 days. Following 5 days of pretreatment with E2, they were injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on the sixth day. The brains were collected on day 11. Immunohistochemistry and quantitative study were used to assess the number of tyrosine hydroxylase-immunoreactive (TH-IR) neurons in the substantia nigra pars compacta (SNpc) and that of activated astrocytes and activated microglia in the SNpc and the striatum. Pretreatment with E2 decreased the loss of TH-IR nigral neurons and diminished the deficit of TH-IR striatal fibers triggered by MPTP. The neuroprotective effect of E2 was coincident with an attenuation of a glial response within the nigra and the striatum. These findings suggest that the neuroprotective effects of E2 evidenced in MPTP mouse model might mediate through an inhibition of reactive glia. However, direct neuroprotective effects of E2 upon TH-IR neurons cannot be excluded. © 2006 Elsevier B.V. All rights reserved.
URI: https://ir.swu.ac.th/jspui/handle/123456789/15030
https://www.scopus.com/inward/record.uri?eid=2-s2.0-33646388397&doi=10.1016%2fj.brainres.2006.02.029&partnerID=40&md5=5c0a295fc660ce656359267fbace76bb
ISSN: 68993
Appears in Collections:Scopus 1983-2021

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