Title:Neuroinflammatory Response and Redox-regulation Activity of
Hyperoside in Manganese-induced Neurotoxicity Model of Wistar Rats
Volume: 17
Issue: 3
Author(s): Olalekan Bukunmi Ogunro*Oluwaseun Ruth Olasehinde
Affiliation:
- Department of Biological Sciences, Reproductive & Endocrinology, Toxicology, and Bioinformatics Research
Laboratory, KolaDaisi University, Ibadan, Nigeria
- Department of Biochemistry, University of Ilorin, Ilorin, Nigeria
Keywords:
Alzheimer’s disease, Gongronema latifolium, neurodegenerative diseases, Dementias, Cognition disorder, Neurotransmitter.
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 Gongronema latifolium (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 MnCl2 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 MnCl2-induced memory impairment, organ-body
weight discrepancies, and fluid intake deficits. Exposure to MnCl2 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, H2O2, 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 MnCl2 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 MnCl2.
Conclusion: In summary, HELEGL reversed the causative factors of neurodegenerative diseases
induced by MnCl2 exposure, suggesting its potential for further exploration as a prospective
therapeutic agent in the management of Alzheimer's disease and related forms of dementia.
