Evidence map›Paper›PMID 40454497›Full record

ArticleCurrent neuropharmacology2025

Quercetin Protects against Ethanol-induced Neurodegeneration in Adult Rat Cortex.

Haroon Badshah, Rehman Zafar, Heeyoung Kang, Sangbae Ma, Haroon Khan, Myeong Ok Kim

Abstract read
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Article in Current neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Haroon BadshahDivision of Life Sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju, 52828, Korea.
Rehman ZafarDepartment of Pharmaceutical Chemistry, Faculty of Pharmaceutical Sciences, Riphah International University, Islamabad, Pakistan.
Heeyoung KangDepartment of Neurology, Gyeongsang National University Hospital & College of Medicine, Gyeongsang National University, Changwon, Jinju, 52727, Republic of Korea.
Sangbae MaAI Biotics Co., Hwaseong-si, Gyeonggido, Republic of Korea.
Haroon KhanDepartment of Pharmacy, Abdul Wali Khan University Mardan, Mardan, 23200, Pakistan.
Myeong Ok KimDivision of Life Sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju, 52828, Korea.

Funding

Bio & Medical Technology Development Program of the National Research Foundation (NRF) by the Korean Government (MSIT) RS-2024-00441331
6 · The paper itself

Abstract

introductionQuercetin, a naturally occurring flavonoid, has been reported to possess several pharmacological activities including neuroprotective properties. Chronic alcohol exposure is known to cause apoptotic neurodegeneration. In this study, docking studies were used to investigate the ligand-protein affinity against various neuroinflammatory targets like ChAt, TNF, IL-6, and IL-1β. Next, molecular studies were performed to determine quercetin activity against chronic ethanol- induced neurodegeneration in the adult rat cortex.

methodsAdult rats were treated with ethanol for 3 months while quercetin was treated for the last 20 days along with ethanol to the respective experimental groups. Elements of the mitochondrial apoptotic pathway i.e. pro-apoptotic protein Bax, cytochrome C release, and activation of caspase-9 and caspase-3 were determined after respective drug treatment. Our docking results revealed that quercetin possesses neuroprotective potential by targeting neuroinflammatory proteins inhibiting neurodegeneration.

resultsWestern blot results showed that ethanol administration increased the protein expressions of Bax, cytochrome C, caspase-9, and caspase-3. Furthermore, DNA damage was also observed by chronic ethanol treatment with increased expression of PARP-1. Quercetin treatment offered neuroprotection in the cortex against ethanol-induced neurodegeneration. Quercetin reversed the ethanolinduced apoptotic trend via down-regulating Bax, preventing cytochrome C release and inhibition of caspase cascade.

conclusionImmunohistological findings i.e. caspase-3 immunoreactivity, Nissl staining, and Fluoro- Jade B staining also revealed significant neuronal survival with quercetin treatment against ethanol- induced neuronal cell death. Our in-silico and in-vivo findings suggest that quercetin has the potential capability to be used as a neuroprotective agent against alcoholic neurotoxicity.

Indexed as

Cerebral CortexEthanolNeuroprotective AgentsQuercetinAnimalsApoptosisMaleMolecular Docking SimulationRatsRats, Sprague-DawleyEthanolNeuroprotective AgentsQuercetinethanolmitochondrial apoptotic pathwaymolecular dockingneurodegenerationQuercetintherapeutic potential.

Identifiers

PMID40454497
PMCPMC12645135

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