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Tetramethylpyrazine Protects Neurons from Oxygen-Glucose Deprivation-Induced Death

BACKGROUND: To explore the theoretical basis for protecting the brain from ischemic stroke with tetramethylpyrazine, we studied whether and how tetramethylpyrazine could protect neurons against the oxygen-glucose deprivation (OGD)-induced death and whether transient receptor potential cation channel...

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Detalles Bibliográficos
Autores principales: Shao, Zhengkai, Wang, Lijun, Liu, Shuang, Wang, Xuefeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5685034/
https://www.ncbi.nlm.nih.gov/pubmed/29104282
http://dx.doi.org/10.12659/MSM.904554
Descripción
Sumario:BACKGROUND: To explore the theoretical basis for protecting the brain from ischemic stroke with tetramethylpyrazine, we studied whether and how tetramethylpyrazine could protect neurons against the oxygen-glucose deprivation (OGD)-induced death and whether transient receptor potential cation channel, subfamily C, member 6 (TRPC6) was involved. MATERIAL/METHODS: Primary rat cortical neurons were cultured and an OGD model was established in the presence or absence of tetramethylpyrazine. Neuronal death was assessed by measuring the uptake of membrane-impermeable PI. Western blot analysis was used to determine the protein expressions of TRPC6 and caspase-3. The involvement of TRPC6 was tested via RNAi against TRPC6. RESULTS: OGD-induced neuronal death was decreased by tetramethylpyrazine in a concentration-dependent manner. The expression of TRPC6 protein was decreased by OGD. Furthermore, downregulating TRPC6 by RNA interfering mimicked the effect of OGD in neuronal death. Tetramethylpyrazine attenuated OGD-induced TRPC6 downregulation in a tetramethylpyrazine concentration-dependent manner. However, these effects of tetramethylpyrazine on attenuating OGD-induced neuronal death were abolished by TRPC6 RNAi. CONCLUSIONS: Tetramethylpyrazine can protect neurons from oxygen-glucose deprivation-induced death, possibly via TRPC6.