Relationship between the MAPK/ERK pathway and neurocyte apoptosis after cerebral infarction in rats

Q.-C. Wang, L. Lu, H.-J. Zhou

Department of Neurology and Neurosurgery, The Third Affiliated Hospital of Chongqing Medical University (Gener Hospital), Chongqing, China. pbhg94@163.com

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• Neurology

OBJECTIVE: The aim of this study was to explore the relationship between the mitogen-activated protein kinase (MAPK)/extracellular regulated protein kinase (ERK) pathway and neurocyte apoptosis after cerebral infarction in rats.
MATERIALS AND METHODS: Neural stem cells were isolated from rats by establishing the cerebral infarction model and sham model. Isolated cells were cultured in complete culture medium in vitro. Real-time quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was used to detect the messenger ribonucleic acid (mRNA) expression of ERK1 and ERK2 in the MARK pathway. Western blotting was applied to examine the activation of the MAPK/ERK pathway and neuron-specific markers. The expression of neuron-specific enolase (NSE) was detected via immunofluorescence. Cell activity and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively.
RESULTS: The mRNA expressions of ERK1 and ERK2 in neural stem cells increased in a time-dependent manner after cerebral infarction in rats. The expressions of ERK1, ERK2, cyclin D1, Nestin, NSE and glial fibrillary acidic-protein (GFAP) in neural stem cells were significantly decreased after being treated with SCH772984. Cell activity, proliferation and differentiation were markedly inhibited. However, cleaved-caspase 3 protein and apoptosis rate were remarkably increased.
CONCLUSIONS: The MAPK/ERK pathway seriously affects neurocyte apoptosis after cerebral infarction in rats. When the MAPK/ERK pathway is inhibited, neurocyte apoptosis is remarkably increased after cerebral infarction in rats.

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