Diego V Beckmann1, Fabiano B Carvalho2, Cinthia M Mazzanti3, Rosmarini P Dos Santos1, Amanda O Andrades1, Graciane Aiello1, Angel Rippilinger1, Dominguita L Graça2, Fátima H Abdalla4, Lizielle S Oliveira4, Jessié M Gutierres4, Maria Rosa C Schetinger4, Alexandre Mazzanti5. 1. Laboratório de Cirurgia Experimental (LACE), Centro de Ciências Rurais, Universidade Federal de Santa Maria, Santa Maria, RS 97105-900, Brazil. 2. Setor de Bioquímica e Biologia Molecular do Laboratório de Terapia Celular, Centro de Ciências Rurais, Universidade Federal de Santa Maria, Santa Maria, RS 97105-900, Brazil. 3. Setor de Bioquímica e Biologia Molecular do Laboratório de Terapia Celular, Centro de Ciências Rurais, Universidade Federal de Santa Maria, Santa Maria, RS 97105-900, Brazil. Electronic address: cmelazzomazzanti@gmail.com. 4. Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS 97105-900, Brazil. 5. Laboratório de Cirurgia Experimental (LACE), Centro de Ciências Rurais, Universidade Federal de Santa Maria, Santa Maria, RS 97105-900, Brazil. Electronic address: alexamazza@yahoo.com.br.
Abstract
AIM: The purpose of this study was to investigate whether the flavonoid quercetin can prevent alterations in the behavioral tests and of cholinergic neurotransmission in rats submitted to the ethidium bromide (EB) experimental demyelination model during events of demyelination and remyelination. MAIN METHODS: Wistar rats were randomly distributed into four groups (20 animals per group): Control (pontine saline injection and treatment with ethanol), Querc (pontine saline injection and treatment with quercetin), EB (pontine 0.1% EB injection and treatment with ethanol), and EB+Querc (pontine 0.1% EB injection and treatment with quercetin). The groups Querc and Querc+EB were treated once daily with quercetin (50mg/kg) diluted in 25% ethanol solution (1ml/kg) and the animals of the control and EB groups were treated once daily with 25% ethanol solution (1ml/kg). Two stages were observed: phase of demyelination (peak on day 7) and phase of remyelination (peak on day 21 post-injection). Behavioral tests (beam walking, foot fault and inclined plane test), acetylcholinesterase (AChE) activity and lipid peroxidation in pons, cerebellum, hippocampus, hypothalamus, striatum and cerebral cortex were measured. KEY FINDINGS: The quercetin promoted earlier locomotor recovery, suggesting that there was demyelination prevention or further remyelination velocity as well as it was able to prevent the inhibition of AChE activity and the increase of lipidic peroxidation, suggesting that this compound can protect cholinergic neurotransmission. SIGNIFICANCE: These results may contribute to a better understanding of the neuroprotective role of quercetin and the importance of an antioxidant diet in humans to provide benefits in neurodegenerative diseases such as MS.
AIM: The purpose of this study was to investigate whether the flavonoidquercetin can prevent alterations in the behavioral tests and of cholinergic neurotransmission in rats submitted to the ethidium bromide (EB) experimental demyelination model during events of demyelination and remyelination. MAIN METHODS:Wistar rats were randomly distributed into four groups (20 animals per group): Control (pontine saline injection and treatment with ethanol), Querc (pontine saline injection and treatment with quercetin), EB (pontine 0.1% EB injection and treatment with ethanol), and EB+Querc (pontine 0.1% EB injection and treatment with quercetin). The groups Querc and Querc+EB were treated once daily with quercetin (50mg/kg) diluted in 25% ethanol solution (1ml/kg) and the animals of the control and EB groups were treated once daily with 25% ethanol solution (1ml/kg). Two stages were observed: phase of demyelination (peak on day 7) and phase of remyelination (peak on day 21 post-injection). Behavioral tests (beam walking, foot fault and inclined plane test), acetylcholinesterase (AChE) activity and lipid peroxidation in pons, cerebellum, hippocampus, hypothalamus, striatum and cerebral cortex were measured. KEY FINDINGS: The quercetin promoted earlier locomotor recovery, suggesting that there was demyelination prevention or further remyelination velocity as well as it was able to prevent the inhibition of AChE activity and the increase of lipidic peroxidation, suggesting that this compound can protect cholinergic neurotransmission. SIGNIFICANCE: These results may contribute to a better understanding of the neuroprotective role of quercetin and the importance of an antioxidant diet in humans to provide benefits in neurodegenerative diseases such as MS.