Neurobehavioral and Immune-Histochemical Effects of Daucus Carota Ethanolic Leaf Extract in Cadmium-Induced Toxicity of the Hippocampus and Prefrontal Cortex of Adult Wistar Rats
by Agatha Nkechinyere Ekechi, Albert N. Eteudo, Chijioke Stanley Anyigor-Ogah, Clinton Ogbonna Njoku, Idika Mba Idika, Miracle Erinma Chukwuonye, Ndudim Ogwuegbu Okezie, Okechukwu Anyigor-Ogah, Toochukwu Nnamdi Nnama
Published: September 18, 2025 • DOI: 10.51244/IJRSI.2025.120800187
Abstract
Introduction: Chronic exposure to cadmium has been linked to neuro-degenerative disorders due to its ability to induce neuro-inflammation and apoptosis in critical brain regions such as the hippocampus and prefrontal cortex.
Objectives: This study evaluated the neurobehavioral and immune-histochemical effects of Daucus carota ethanolic leaf extract (CLE) in cadmium-induced toxicity of the hippocampus and prefrontal cortex of adult wistar rats.
Materials and methods: Thirty adult male Wistar rats (weighing 150–180g) were assigned into five groups (6 per group). Group 1 (normal control) received water, Group 2 (Cadmium-only) received cadmium chloride (5 mg/kg). Group 3 received only CLE (400 mg/kg). Groups 4 and 5 received cadmium chloride and CLE at doses of 200 mg/kg and 400 mg/kg, respectively. Neuro-behavioral tests were conducted to assess cognitive and emotional responses. Brain tissues were harvested for biochemical analysis as well as immune-histochemical evaluation of neuronal integrity. Data were analyzed using GraphPad Prism version 8 and presented as Mean ± SEM. Statistical comparisons were made using one-way ANOVA followed by Tukey’s post hoc test, with significance set at p < 0.05.
Results: Cadmium exposure significantly impaired cognitive function and triggered neuro-inflammation. Group C showed weight loss compared to the control group, indicating systemic toxicity. However, CLE treatment ameliorated these changes in a dose-dependent manner. The Cadmium + CLE (200 mg/kg) and Cadmium + CLE (400 mg/kg) groups exhibited significant improvements compared to the Cadmium-only group. The highest dose (400 mg/kg) demonstrated the most pronounced neuroprotective effects, with weight parameters approaching those of the control group. Histamine level were lowered significantly in group B when compared to the control group A at p<0.05, acetylcholine level was significantly lowered in all the treated groups when compared to group B at p<0.05.
Conclusion: The CLE exhibits potent neuroprotective properties against cadmium-induced neurotoxicity, hence could serve as a promising natural intervention for mitigating heavy metal-induced cognitive and neuronal impairments.