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Ameliorative effect of vinpocetine on brain toxicity in rats treated with acrylamide

2026 · Open Journal of Physiology and Pharmacology · 0 citations

TL;DR

Vinpocetine administration ameliorated hematological disturbances, oxidative damage, and histological alterations resulting from AC administration, suggesting that vinpocetine has a protective action against AC-induced neural damage.

Abstract

Background: Acrylamide (AC) is a highly reactive carbonyl compound widely used in industrial processes, having oxidative stress, neurotoxicity, and genotoxicity properties. Vinpocetine has been reported to exhibit neuroprotective, antioxidant, and anti-inflammatory properties. Aim: The study aims to evaluate vinpocetine’s protective effects in mitigating AC-induced toxicity in male albino rats. Methods: In the current research, 24 rats were used, arranged into 4 groups as follows: normal untreated group, Vinpo. group (5 mg/kg b.wt), AC group (38.27 mg/kg b.wt), Vinpo. + AC group (received Vinpo. and after one hour received a dose of AC). At the end of the experimental period, blood samples and brain specimens were collected from each rat to assess hematological and biochemical parameters and to conduct histopathological and immunohistochemical analyses. Results: AC administration caused a marked reduction in hematological parameters, reduced glutathione (GSH), superoxide dismutase (SOD), and brain-derived neurotrophic factor (BDNF). Also resulted in a marked reduction in key neurotransmitters (serotonin, dopamine, and acetylcholine (ACH)) as an indicator for oxidative stress and toxicity. Lipid peroxidation markers, like malondialdehyde (MDA), increase as an indicator of oxidative injury. The histological structural abnormalities and enhancement in the level of cleaved caspase-3 indicated the damage in brain tissues. Conclusion: Vinpocetine administration ameliorated hematological disturbances, oxidative damage, and histological alterations resulting from AC administration. These findings suggest that vinpocetine has a protective action against AC-induced neural damage.

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