Morphine reverses the effects of 1-methyl-4-phenylpyridinium in PC12 cells through activating PI3K/Akt.
Int J Neurosci
; 129(1): 30-35, 2019 Jan.
Article
em En
| MEDLINE
| ID: mdl-29936883
ABSTRACT
AIM OF THE STUDY Parkinson's disease (PD) is a neurodegenerative disorder. It is caused by the degeneration of dopaminergic neurons and the dopamine (DA) deletion in the substantia nigra pars compacta (SNpc). Morphine elevates the level of dopamine in the mesolimbic dopamine system and plays a role in alleviating PD symptoms. However, the molecular mechanism is still unclear. The aim of the study is to investigate the mechanism on morphine alleviating PD symptoms. MATERIALS AND METHODS:
The viability of PC12 cells was measured by using MTT assay. The expressions of tyrosine hydroxylase (TH), thioredoxin-1 (Trx-1), CyclinD1 and Cyclin-dependent kinase5 (Cdk5) were detected by Western Blot.RESULTS:
In present study, we found that morphine increased the cell viability in PC12 cells. 1-methyl-4-phenylpyridi-nium (MPP+) reduced the cell viability and TH expression, which were reversed by morphine. MPP+ decreased the expressions of Trx-1, CyclinD1, Cdk5, which were restored by morphine. Moreover, the role of morphine in restoring the expressions of Trx-1, CyclinD1 and Cdk5 decreased by MPP+ was abolished by LY294002, phosphatidylinositol-3-kinase (PI3K)/Akt inhibitor.CONCLUSIONS:
These results suggest that morphine reverses effects induced by MPP þ through activating PI3K/Akt pathway.Palavras-chave
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Doença de Parkinson
/
1-Metil-4-fenilpiridínio
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Fosfatidilinositol 3-Quinases
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Proteínas Proto-Oncogênicas c-akt
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Morfina
Limite:
Animals
Idioma:
En
Revista:
Int J Neurosci
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
China