Quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity

The rotenone-induced animal model of Parkinson’s disease (PD) has been used to investigate the pathogenesis of PD. Oxidative stress is one of the main contributors of neurodegeneration in PD. Flavonoids have the potential to modulate neuronal function and combat various neurodegenerative diseases. T...

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Autores principales:	Syeda Madiha, Zehra Batool, Saiqa Tabassum, Laraib Liaquat, Sadia Sadir, Sidrah Shahzad, Fizza Naqvi, Sadia Saleem, Sarwat Yousuf, Amber Nawaz, Saara Ahmad, Irfan Sajid, Asia Afzal, Saida Haider
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/4bc3f11249cf4f2b8957fa3600c60144
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spelling	oai:doaj.org-article:4bc3f11249cf4f2b8957fa3600c601442021-11-25T06:11:05ZQuercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity1932-6203https://doaj.org/article/4bc3f11249cf4f2b8957fa3600c601442021-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8589152/?tool=EBIhttps://doaj.org/toc/1932-6203The rotenone-induced animal model of Parkinson’s disease (PD) has been used to investigate the pathogenesis of PD. Oxidative stress is one of the main contributors of neurodegeneration in PD. Flavonoids have the potential to modulate neuronal function and combat various neurodegenerative diseases. The pre- and post-supplementation of quercetin (50 mg/kg, p.o) was done in rats injected with rotenone (1.5 mg/kg, s.c). After the treatment, behavioral activities were monitored for motor activity, depression-like behavior, and cognitive changes. Rats were decapitated after behavioral analysis and the brain samples were dissected out for neurochemical and biochemical estimation. Results showed that supplementation of quercetin significantly (p<0.01) restored rotenone-induced motor and non-motor deficits (depression and cognitive impairments), enhanced antioxidant enzyme activities (p<0.01), and attenuated neurotransmitter alterations (p<0.01). It is suggested that quercetin supplementation improves neurotransmitter levels by mitigating oxidative stress via increasing antioxidant enzyme activity and hence improves motor activity, cognitive functions, and reduces depressive behavior. The results of the present study showed that quercetin pre-supplementation produced more significant results as compared to post-supplementation. These findings show that quercetin can be a potential therapeutic agent to reduce the risk and progression of PD.Syeda MadihaZehra BatoolSaiqa TabassumLaraib LiaquatSadia SadirSidrah ShahzadFizza NaqviSadia SaleemSarwat YousufAmber NawazSaara AhmadIrfan SajidAsia AfzalSaida HaiderPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Syeda Madiha Zehra Batool Saiqa Tabassum Laraib Liaquat Sadia Sadir Sidrah Shahzad Fizza Naqvi Sadia Saleem Sarwat Yousuf Amber Nawaz Saara Ahmad Irfan Sajid Asia Afzal Saida Haider Quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity
description	The rotenone-induced animal model of Parkinson’s disease (PD) has been used to investigate the pathogenesis of PD. Oxidative stress is one of the main contributors of neurodegeneration in PD. Flavonoids have the potential to modulate neuronal function and combat various neurodegenerative diseases. The pre- and post-supplementation of quercetin (50 mg/kg, p.o) was done in rats injected with rotenone (1.5 mg/kg, s.c). After the treatment, behavioral activities were monitored for motor activity, depression-like behavior, and cognitive changes. Rats were decapitated after behavioral analysis and the brain samples were dissected out for neurochemical and biochemical estimation. Results showed that supplementation of quercetin significantly (p<0.01) restored rotenone-induced motor and non-motor deficits (depression and cognitive impairments), enhanced antioxidant enzyme activities (p<0.01), and attenuated neurotransmitter alterations (p<0.01). It is suggested that quercetin supplementation improves neurotransmitter levels by mitigating oxidative stress via increasing antioxidant enzyme activity and hence improves motor activity, cognitive functions, and reduces depressive behavior. The results of the present study showed that quercetin pre-supplementation produced more significant results as compared to post-supplementation. These findings show that quercetin can be a potential therapeutic agent to reduce the risk and progression of PD.
format	article
author	Syeda Madiha Zehra Batool Saiqa Tabassum Laraib Liaquat Sadia Sadir Sidrah Shahzad Fizza Naqvi Sadia Saleem Sarwat Yousuf Amber Nawaz Saara Ahmad Irfan Sajid Asia Afzal Saida Haider
author_facet	Syeda Madiha Zehra Batool Saiqa Tabassum Laraib Liaquat Sadia Sadir Sidrah Shahzad Fizza Naqvi Sadia Saleem Sarwat Yousuf Amber Nawaz Saara Ahmad Irfan Sajid Asia Afzal Saida Haider
author_sort	Syeda Madiha
title	Quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity
title_short	Quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity
title_full	Quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity
title_fullStr	Quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity
title_full_unstemmed	Quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity
title_sort	quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/4bc3f11249cf4f2b8957fa3600c60144
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Quercetin exhibits potent antioxidant activity, restores motor and non-motor deficits induced by rotenone toxicity

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