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Quercetin attenuates the reduction of parvalbumin in middle cerebral artery occlusion animal model

BACKGROUND: Calcium is a critical factor involved in modulation of essential cellular functions. Parvalbumin is a calcium buffering protein that regulates intracellular calcium concentrations. It prevents rises in calcium concentrations and inhibits apoptotic processes during ischemic injury. Querce...

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Detalles Bibliográficos
Autores principales: Park, Dong-Ju, Kang, Ju-Bin, Shah, Fawad-Ali, Koh, Phil-Ok
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905853/
https://www.ncbi.nlm.nih.gov/pubmed/33632310
http://dx.doi.org/10.1186/s42826-021-00086-0
Descripción
Sumario:BACKGROUND: Calcium is a critical factor involved in modulation of essential cellular functions. Parvalbumin is a calcium buffering protein that regulates intracellular calcium concentrations. It prevents rises in calcium concentrations and inhibits apoptotic processes during ischemic injury. Quercetin exerts potent antioxidant and anti-apoptotic effects during brain ischemia. We investigated whether quercetin can regulate parvalbumin expression in cerebral ischemia and glutamate toxicity-induced neuronal cell death. Adult male rats were treated with vehicle or quercetin (10 mg/kg) 30 min prior to middle cerebral artery occlusion (MCAO) and cerebral cortical tissues were collected 24 h after MCAO. We used various techniques including Western blot, reverse transcription-PCR, and immunohistochemical staining to elucidate the changes of parvalbumin expression. RESULTS: Quercetin ameliorated MCAO-induced neurological deficits and behavioral changes. Moreover, quercetin prevented MCAO-induced a decrease in parvalbumin expression. CONCLUSIONS: These findings suggest that quercetin exerts a neuroprotective effect through regulation of parvalbumin expression.