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Prefrontal cortical morphology of nickel chloride induced toxicity following the administration of Moringa oleifera aqueous extract
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Abstract
Introduction and Aim: Heavy metal exposure, particularly to nickel chloride (NiCl₂), poses significant health risks due to its neurotoxic effects, especially on the prefrontal cortex (PFC), a critical region for cognition and decision-making. NiCl₂ induces oxidative stress, neuronal damage, and inflammation, necessitating effective therapeutic interventions. Moringa oleifera, known for its antioxidant and neuroprotective properties, is a promising natural remedy. This study aimed to investigate the effects of NiCl₂-induced toxicity on PFC morphology in Wistar rats and evaluate the ameliorative potential of M. oleifera aqueous extract.
Methodology: Twenty-five adult male Wistar rats were divided into five groups (n=5): normal control (food and water), NiCl₂-untreated (20 mg/kg NiCl₂), M. oleifera-only (2500 mg/kg), NiCl₂ + 1250 mg/kg M. oleifera, and NiCl₂ + 2500 mg/kg M. oleifera, all administered orally for 14 days. Body weights were recorded, and PFC tissues were harvested for histological (H&E), Nissl (Cresyl Fast Violet), and immunohistochemical (GFAP) analyses. Data were analysed using one-way and two-way ANOVA with post-tests (p<0.05).
Results: NiCl₂ exposure reduced body weight and induced PFC neuronal degeneration, inflamed blood vessels, intense Nissl staining, and astrogliosis, indicating neurotoxicity. M. oleifera-only group showed normal PFC morphology. Groups treated with M. oleifera (1250 mg/kg) exhibited improved neuronal integrity and reduced inflammation, while the 2500 mg/kg group showed partial vascular enlargement and severe astrogliosis. No significant body weight differences were observed.
Conclusion: NiCl₂ induces significant PFC neurotoxicity, which M. oleifera, particularly at 1250 mg/kg, mitigates by preserving neuronal structure and reducing inflammation, likely via antioxidant mechanisms. Higher doses (2500 mg/kg) may be less effective due to increased astrogliosis. M. oleifera holds therapeutic potential for heavy metal-induced neurotoxicity, warranting further dose optimisation studies.
Springer Science and Business Media LLC
Title: Prefrontal cortical morphology of nickel chloride induced toxicity following the administration of Moringa oleifera aqueous extract
Description:
Abstract
Introduction and Aim: Heavy metal exposure, particularly to nickel chloride (NiCl₂), poses significant health risks due to its neurotoxic effects, especially on the prefrontal cortex (PFC), a critical region for cognition and decision-making.
NiCl₂ induces oxidative stress, neuronal damage, and inflammation, necessitating effective therapeutic interventions.
Moringa oleifera, known for its antioxidant and neuroprotective properties, is a promising natural remedy.
This study aimed to investigate the effects of NiCl₂-induced toxicity on PFC morphology in Wistar rats and evaluate the ameliorative potential of M.
oleifera aqueous extract.
Methodology: Twenty-five adult male Wistar rats were divided into five groups (n=5): normal control (food and water), NiCl₂-untreated (20 mg/kg NiCl₂), M.
oleifera-only (2500 mg/kg), NiCl₂ + 1250 mg/kg M.
oleifera, and NiCl₂ + 2500 mg/kg M.
oleifera, all administered orally for 14 days.
Body weights were recorded, and PFC tissues were harvested for histological (H&E), Nissl (Cresyl Fast Violet), and immunohistochemical (GFAP) analyses.
Data were analysed using one-way and two-way ANOVA with post-tests (p<0.
05).
Results: NiCl₂ exposure reduced body weight and induced PFC neuronal degeneration, inflamed blood vessels, intense Nissl staining, and astrogliosis, indicating neurotoxicity.
M.
oleifera-only group showed normal PFC morphology.
Groups treated with M.
oleifera (1250 mg/kg) exhibited improved neuronal integrity and reduced inflammation, while the 2500 mg/kg group showed partial vascular enlargement and severe astrogliosis.
No significant body weight differences were observed.
Conclusion: NiCl₂ induces significant PFC neurotoxicity, which M.
oleifera, particularly at 1250 mg/kg, mitigates by preserving neuronal structure and reducing inflammation, likely via antioxidant mechanisms.
Higher doses (2500 mg/kg) may be less effective due to increased astrogliosis.
M.
oleifera holds therapeutic potential for heavy metal-induced neurotoxicity, warranting further dose optimisation studies.
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