Adansonia digitata L. leaf extract attenuates lead-induced cortical histoarchitectural changes and oxidative stress in the prefrontal cortex of adult male Wistar rats
Autor: | Godswill Ezemeka, Chris, Kate Nebo, E.A. Esom, Chike Anibeze, Ben-Azu Benneth, Vivian O Atuadu, John Chukwuma Oyem |
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Rok vydání: | 2020 |
Předmět: |
medicine.medical_specialty
010501 environmental sciences medicine.disease_cause 01 natural sciences Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound Internal medicine medicine Pharmacology (medical) General Pharmacology Toxicology and Pharmaceutics Prefrontal cortex 030304 developmental biology 0105 earth and related environmental sciences 0303 health sciences biology Neurotoxicity Malondialdehyde medicine.disease biology.organism_classification Endocrinology chemistry Catalase Lead acetate biology.protein Adansonia digitata Oxidative stress |
Zdroj: | Drug Metabolism and Drug Interactions. 36:63-71 |
ISSN: | 2191-0162 0792-5077 |
DOI: | 10.1515/dmpt-2020-0116 |
Popis: | Objectives Adansonia digitata L. is popularly known for the management of various neurological diseases in ethno-medicine. Studies have shown that lead toxicity is a possible risk factor for early onset of neurodegenerative disease. Hence, this study was designed to evaluate the effect of A. digitata aqueous leaf extract (ADALE) against lead-induced oxidative stress and histo-architectural changes in the prefrontal cortex of adult Wistar rats. Methods Saline (10 mL/kg), ADALE (500 and 1000 mg/kg) and EDTA (55 mg/kg) were pretreated orally 30 min prior to lead acetate (LA) (120 mg/kg) administration to male Wistar rats (n=7) for 21 days. Thereafter, standard biochemical (superoxide dismutate, catalase, glutathionxe and malondialdehyde), histological (H&E) and histochemical assessment (crystyl fast violet stain for nissil substance) were carried out in the prefrontal cortex. Results ADALE significantly (p Conclusions The result of this study showed that A. digitata aqueous leaf extract attenuated lead acetate-induced cortical neurodegeneration via inhibition of oxidative stress. |
Databáze: | OpenAIRE |
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