The Possible Role of Naringenin in the Prevention of Alcohol-Induced Neurochemical and Neurobehavioral Deficits.

Autor: Soliman NA; Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta, Egypt., Abdel Ghafar MT; Department of Clinical Pathology, Faculty of Medicine, Tanta University, Aljaysh St, Medical Campus, Tanta, 31511, Egypt. mohammedtarek5514@yahoo.com., AbuoHashish NA; Department of Pharmacology, Faculty of Medicine, Tanta University, Tanta, Egypt., Ibrahim MA; Department of Histology, Faculty of Medicine, Tanta University, Tanta, Egypt., Eid AM; Department of Pathology, Faculty of Medicine, Tanta University, Tanta, Egypt., El-Gohary RM; Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta, Egypt., Abo El Gheit RE; Department of Physiology Faculty of Medicine, Tanta University, Tanta, Egypt., Elshamy AM; Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta, Egypt.
Jazyk: angličtina
Zdroj: Neurochemical research [Neurochem Res] 2023 Feb; Vol. 48 (2), pp. 537-550. Date of Electronic Publication: 2022 Oct 15.
DOI: 10.1007/s11064-022-03775-x
Abstrakt: Chronic alcohol consumption is associated with progressive/irreversible neurodegeneration. However, there is not a clear understanding of its discrete pathophysiology or therapeutic intervention. The present study aimed to investigate the protective effect of the natural citrus flavonoid, naringenin (NAG), against alcohol-induced neurodegeneration in the brain cerebral cortex. Thirty-two male albino rats were randomly divided into four equal groups (eight rats each): control group (I); NAG-treated group (II); alcohol-intoxicated group (III) and alcohol + NAG co-treated group (IV). Brain nuclear factor erythroid 2-related factor 2 and receptor-interacting protein kinase 3 expression were assessed by real-time polymerase chain reaction. NAD(P)H quinone oxidoreductase 1 activity and malondialdehyde, reduced glutathione, mixed lineage kinase-like protein, phosphorylated glycogen synthase kinase 3 beta, and ciliary neurotrophic factor levels were all measured biochemically. B-cell lymphoma 2 expression was assessed by immunohistochemistry. A histopathological examination and neurobehavioral tests were performed. The alcohol-treated group showed a significant increase in oxidative stress and necroptosis biomarkers with a significant reduction in neuroprotective proteins. NAG co-administration effectively ameliorated cognitive dysfunction with an apparent neuroprotective effect by targeting various signaling pathways, including nuclear factor erythroid 2-related factor/NAD(P)H quinone oxidoreductase 1, anti-oxidant capacity, attenuated necroptosis, and upregulated neuroprotective ciliary neurotrophic factor. The study findings suggest NAG as a possible management strategy for alcohol-induced neurodegeneration.
(© 2022. The Author(s).)
Databáze: MEDLINE
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