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Quercetin attenuates the reduction of parvalbumin in middle cerebral artery occlusion animal model
- Source :
- Laboratory Animal Research, Laboratory Animal Research, Vol 37, Iss 1, Pp 1-8 (2021)
- Publication Year :
- 2020
-
Abstract
- 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.
- Subjects :
- 0301 basic medicine
Calcium buffering
Ischemia
chemistry.chemical_element
Pharmacology
Calcium
Neuroprotection
Calcium in biology
Brain ischemia
03 medical and health sciences
0302 clinical medicine
medicine
heterocyclic compounds
lcsh:QH301-705.5
Parvalbumin
lcsh:R5-920
biology
Chemistry
Research
Glutamate receptor
Cerebral ischemia
medicine.disease
030104 developmental biology
lcsh:Biology (General)
nervous system
biology.protein
Quercetin
lcsh:Medicine (General)
030217 neurology & neurosurgery
Subjects
Details
- ISSN :
- 17386055
- Volume :
- 37
- Issue :
- 1
- Database :
- OpenAIRE
- Journal :
- Laboratory animal research
- Accession number :
- edsair.doi.dedup.....345b66f40abccc66f0520f741418f8db