Neuroinflammatory Response and Redox-regulation Activity of Hyperoside in Manganese-induced Neurotoxicity Model of Wistar Rats

Overview

Journal Curr Aging Sci

Publisher Bentham Science Publishers

Specialty Geriatrics

Date 2024 Mar 19

PMID 38500281

Authors

Olalekan Bukunmi Ogunro

Oluwaseun Ruth Olasehinde

Affiliations

Soon will be listed here.

Abstract

Background: Excessive manganese exposure can lead to neurotoxicity with detrimental effects on the brain. Neuroinflammatory responses and redox regulation play pivotal roles in this process. Exploring the impact of hyperoside in a Wistar rat model offers insights into potential neuroprotective strategies against manganese-induced neurotoxicity.

Objective: The study investigated the neuroprotective efficacy of hyperoside isolated from the ethanol leaf extract of (HELEGL), in the brain tissue of Wistar rats following 15 consecutive days of exposure to 30 mg/L of MnCl2.

Methods: Control animals in Group 1 had access to regular drinking water, while animals in groups 2-4 were exposed to MnCl in their drinking water. Groups 3 and 4 also received additional HELEGL at doses of 100 mg/kg and 200 mg/kg of body weight, respectively. In Group 5, HELEGL at a dose of 100 mg/kg of body weight was administered alone. Treatment with HELEGL commenced on day 8 via oral administration.

Results: HELEGL effectively mitigated MnCl-induced memory impairment, organ-body weight discrepancies, and fluid intake deficits. Exposure to MnCl increased the activities or levels of various markers such as acyl peptide hydrolase, tumour necrosis factor-α, dipeptidyl peptidase IV, nitric oxide, IL-1β, prolyl oligopeptidase, caspase-3, myeloperoxidase, HO, and malondialdehyde, while it decreased the activities or levels of others, including AChE, BChE, DOPA, serotonin, epinephrine, norepinephrine, GST, GPx, CAT, SOD, GSH, and T-SH (p < 0.05). In contrast, HELEGL effectively counteracted the adverse effects of MnCl by alleviating oxidative stress, inflammation, apoptosis, mitochondrial dysfunction, cognitive deficits, and bolstering the antioxidant status. Moreover, HELEGL restored the normal histoarchitecture of the brain, which had been distorted by MnCl.

Conclusion: In summary, HELEGL reversed the causative factors of neurodegenerative diseases induced by MnCl exposure, suggesting its potential for further exploration as a prospective therapeutic agent in the management of Alzheimer's disease and related forms of dementia.

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