Neuroprotective Effect of Quercetin and Memantine against AlCl3-Induced Neurotoxicity in Albino Wistar Rats

Abstract

Recent evidences indicate that there is a substantial increase in worldwide cases of dementia. Alzheimer's disease is the leading cause of dementia and may contribute to 60–70% of cases. Quercetin is a unique bioflavonoid that has numerous therapeutic benefits such as anti-allergy, anti-ulcer, anti-inflammatory, anti-hypertensive, anti-cancer, immuno-modulatory, anti-infective, antioxidant, acetylcholinesterase inhibitory activity, neuroprotective effects, etc. In the present study, we evaluated the neuroprotective effect of orally administered quercetin with memantine in albino Wistar rats after inducing neurotoxicity through AlCl3 (100 mg/kg, p.o.). Chronic administration of AlCl3 resulted in poor retention of memory and significant oxidative damage. Various behavioral parameters, such as locomotor activity, Morris water maze, elevated plus maze, and passive avoidance test, were assessed on days 21 and 42 of the study. The animals were euthanatized following the completion of the last behavioral assessment. Various oxidative stress parameters were assessed to know the extent of oxidative damage to brain tissue. Quercetin with memantine has shown significant improvement in behavioral studies, inhibition of AChE activity, and reduction in oxidative stress parameters. Histopathological studies assessed for cortex and hippocampus using hematoxylin and eosin (H&E), and Congo red stain demonstrated a reduction in amyloid-β plaque formation after treatment of quercetin with memantine. Immunohistochemistry showed that quercetin with memantine treatment also improved the expression of brain-derived neurotrophic factor (BDNF) and inhibited amyloid-β plaque formation. The present study results demonstrated protective effects of treatment of quercetin with memantine in the neurotoxicity linked to aluminum chloride in albino Wistar rats .

Naringenin, Hesperidin and Quercetin Ameliorate Radiation‐Induced Damage In Rats: In Vivo And In Silico Evaluations

“…[67,68] BChE activity is higher in people with hypertension, obesity, and hyperlipidemia and lower in those who have had myocardial infarctions. [69] BChE impairs neurotransmission, resulting in discomfort for the patient, including nausea, vomiting, fever, impaired vision, and even death. [70] The creation of cholinesterase inhibitors may result in better therapeutic outcomes in the future.…”

“…Therefore, butyrylcholine is crucial for maintaining human health, and its deficiency can result in neurodegenerative disorders [67,68] . BChE activity is higher in people with hypertension, obesity, and hyperlipidemia and lower in those who have had myocardial infarctions [69] . BChE impairs neurotransmission, resulting in discomfort for the patient, including nausea, vomiting, fever, impaired vision, and even death [70] .…”

Biflavonoid quercetin protects against cyclophosphamide–induced organ toxicities via modulation of inflammatory cytokines, brain neurotransmitters, and astrocyte immunoreactivity

“…Also, in this study, quercetin supplementation concentration-dependently increased horizontal locomotion, self grooming and radial arm maze spatial working memory, while at both concentrations of quercetin, an anxiolytic effect and increase in Y maze spatial working memory was observed. Quercetin's ability to reverse brain injury has been reported severally (85)(86)(87)(88)(89)(90).…”

“…Also, in this study, quercetin supplementation concentration-dependently increased horizontal locomotion, self grooming and radial arm maze spatial working memory, while at both concentrations of quercetin, an anxiolytic effect and increase in Y maze spatial working memory was observed. Quercetin’s ability to reverse brain injury has been reported severally (85–90). While most studies have examined its benefits in Alzheimer’s disease, only a few studies have examined its potential benefits in chemotherapy induced neurotoxicity (91).…”

Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction

“…Many drugs used for the treatment of AD depend on the inhibition of acetylcholinesterase, such as galantamine, rivastigmine, and donepezil. This allows for prolonging the action of the deficient neurotransmitter in the brain, but these drugs have side effects with extended use, e.g., hepatotoxicity (Joe and Ringman 2019 ). Therefore, searching for treatments with a high potential to reverse neuronal dysfunction and little risk of side effects and expense will be beneficial.…”