Trévo abrogates Lead Acetate Neurotoxicity in Male Wistar Rats viz Antiamyloidogenesis, Antiglutaminergic, and Anticholinesterase Activities

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dc.contributor.authorAvwioroko, Oghenetega
dc.date.accessioned2022-09-15T12:13:50Z
dc.date.available2022-09-15T12:13:50Z
dc.date.issued2022
dc.description.abstractBackground: Exposure to lead has been linked to biochemical changes similar to those patients suffering from Alzheimer’s disease. Trévo is a phytonutrient-rich product with antiaging and antioxidant properties. Purpose: To investigate the neuroprotective activity of trévo against lead-induced biochemical changes in male Wistar rats. Methods: The study involves 35 animals that were randomly divided into five groups of seven rats each. Group I (Control): Orally administered distilled water; Group II (Induced): Administered 15 mg/kg of lead acetate (PbA) intraperitoneally; Group III (Treatment group): Orally administered 2 mL/kg of trévo for two days before co-administration with PbA for 12 consecutive days; Group IV (Treatment group): Orally administered 5 mL/kg of trévo for two days prior to coadministration with PbA for 12 consecutive days; Group V: Orally administered 5 mL/kg of trévo for 14 consecutive days. Animals were anesthetized with diether and the brain excised and processed for the following biochemical assays: Malonedialdehyde (MDA), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione-Stransferase (GT), acetylcholinesterase (AChE), beta-amyloid, glutamate, Na+/K+ ATPase, and glutamate dehydrogenase (GD). Results: PbA caused significant oxidative stress (increased MDA concentration, decreased GSH concentration, suppressed the activity of CAT, SOD), decreased GT activity, increased activity of AChE, increased the concentration of beta-amyloid, and caused glutamate excitotoxicity (increased concentration of glutamate, decreased activity of Na+/K+ ATPase, and GD) in rat brains. Treatment with trévo at the two different doses significantly prevented oxidative damage, beta-amyloid aggregation, glutamate excitotoxicity, and acetylcholine breakdown induced by lead acetate. Conclusion: Our findings added to the reported pharmacological activity of trévo and supported the antiaging potential of trévoen_US
dc.identifier.issnDOI: 10.1177/09727531221077642
dc.identifier.urihttp://dspace.run.edu.ng:8080/jspui/handle/123456789/3631
dc.language.isoenen_US
dc.publisherAnnals of Neurosciencesen_US
dc.subjectPhytomedicineen_US
dc.subjectHeavy metalsen_US
dc.subjectNeurotoxicityen_US
dc.subjectAcetylcholineen_US
dc.subjectCaspasesen_US
dc.subjectBeta-amyloiden_US
dc.subjectAntioxidanten_US
dc.titleTrévo abrogates Lead Acetate Neurotoxicity in Male Wistar Rats viz Antiamyloidogenesis, Antiglutaminergic, and Anticholinesterase Activitiesen_US
dc.typeArticleen_US
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