Juliet Olayinka1, Anthony Eduviere2, Olusegun Adeoluwa3, Adedamola Fafure4, Adeshina Adebanjo5, Raymond Ozolua6. 1. Neuropharmacology Unit, Department of Pharmacology & Therapeutics, College of Medicine & Health Sciences, Afe-Babalola University, Ado-Ekiti, Nigeria; Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Benin, Benin City 300001, Nigeria. Electronic address: julietolayinka@abuad.edu.ng. 2. Department of Pharmacology & Therapeutics, Faculty of Basic Medical Sciences, Delta State University, Abraka, Nigeria. 3. Neuropharmacology Unit, Department of Pharmacology & Therapeutics, College of Medicine & Health Sciences, Afe-Babalola University, Ado-Ekiti, Nigeria. 4. Department of Anatomy, College of Medicine & Health Sciences, Afe-Babalola University, Ado-Ekiti, Nigeria. 5. Department of Civil Engineering, College of Engineering, Afe-Babalola University, Ado-Ekiti, Nigeria. 6. Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Benin, Benin City 300001, Nigeria.
Abstract
AIMS: Neurodegenerative disorders like Alzheimer's disease (AD) are outcomes of neuroinflammatory processes that result in memory impairment. Quercetin (QT), a plant based flavonoid, has demonstrated notable effects against neurodegeneration and inflammation in models of dementia. However, the underlying mechanisms have not been well elucidated. This study evaluated the possible effects of QT against neuroinflammation and neurodegeneration in scopolamine (SC) induced memory impairment. MAIN METHODS: SC was used to induce memory loss in mice after which novel object recognition test (NORT) was used to assess memory function. Enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the brain tissues of the animals. Brain histology was carried out on the hippocampus (cornus ammonis 1, cornus ammonis 3 and dentate gyrus), and the prefrontal cortex. The population of healthy neuronal cells was counted, using ImageJ software. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) was employed for the identification of cells undergoing apoptosis. KEY FINDINGS: QT reversed memory impairment in the NORT. Increases in TNF-α and IL-6 were attenuated by QT, and histology revealed that QT attenuated SC-induced cell degeneration and death in the hippocampal sub-regions and prefrontal cortex. QT diminished the population of dead cells in SC-treated mice, and also reversed the process of apoptosis induced by SC. SIGNIFICANCE: Findings from the study suggest that QT mitigates pro-inflammatory mediators and reverses neurodegeneration to restore memory function.
AIMS: Neurodegenerative disorders like Alzheimer's disease (AD) are outcomes of neuroinflammatory processes that result in memory impairment. Quercetin (QT), a plant based flavonoid, has demonstrated notable effects against neurodegeneration and inflammation in models of dementia. However, the underlying mechanisms have not been well elucidated. This study evaluated the possible effects of QT against neuroinflammation and neurodegeneration in scopolamine (SC) induced memory impairment. MAIN METHODS: SC was used to induce memory loss in mice after which novel object recognition test (NORT) was used to assess memory function. Enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the brain tissues of the animals. Brain histology was carried out on the hippocampus (cornus ammonis 1, cornus ammonis 3 and dentate gyrus), and the prefrontal cortex. The population of healthy neuronal cells was counted, using ImageJ software. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) was employed for the identification of cells undergoing apoptosis. KEY FINDINGS: QT reversed memory impairment in the NORT. Increases in TNF-α and IL-6 were attenuated by QT, and histology revealed that QT attenuated SC-induced cell degeneration and death in the hippocampal sub-regions and prefrontal cortex. QT diminished the population of dead cells in SC-treated mice, and also reversed the process of apoptosis induced by SC. SIGNIFICANCE: Findings from the study suggest that QT mitigates pro-inflammatory mediators and reverses neurodegeneration to restore memory function.