Neuroprotective Effect of Adansonia digitata Fruit Pulp Extract Against Aluminum Chloride-Induced Memory Deficits and Hippocampal Damage in Rats

Öz

Background: Several reports have shown environmental neuron toxins such as aluminium accumulate in the brain, potentially triggering neurodegenerative disorders. Meanwhile, Adansonia digitata has been shown to possess neuroprotective properties. This study, therefore, assessed the ameliorative properties of Adansonia digitata fruit pulp aqueous extract (AEAD)on aluminum chloride (AlCl3) ¬– induced memory and hippocampal dysfunctions in Wistar rats. The neuroprotective effects were assessed with the Morris water maze for learning and memory, oxidative stress biomarkers glutathione [GSH]), superoxide dismutase [SOD], and (Malondialdehyde [MDA], and histopathological investigation of the CA3 hippocampal region using routine Haematoxylin and Eosin staining techniques. Thirty adult male Wistar rats weighing between 110 and 150 grams were split into six groups at random (n=5). As the Control group, the animals in Group 1 received 2 milliliters per kilogram of distilled water. Group 2 received 100 mg/kg of AlCl3. Ascorbic acid at a dose of 595 mg/kg was given to Group 3. 100 mg/kg AlCl3 and different concentrations of the fruit pulp aqueous extract of Adansonia digitata (500 mg/kg and 1500 mg/kg, respectively) were given to groups 4 and 5. Group 6 received 595 mg/kg of ascorbic acid and 100 mg/kg of AlCl3. Results: The latency time spent to locate the escape platform was observed with remarkable (P<0.05) improvement in the Adansonia digitata fruit pulp aqueous extract treatments compared with the AlCl3-treated group. There was a notable increase in MDA levels and a reduction in SOD and GSH activities in the AlCl3-treated group in relation to the Adansonia digitata fruit pulp aqueous extract-treated groups. Histopathological examination of the CA3 hippocampal region treated with AlCl3 revealed neuronal degenerative changes, whereas, administration of Adansonia digitata fruit pulp aqueous extract ameliorated AlCl3-induced neuronal damages in rats at doses 500mg/kg and 1500mg/kg when compared with the AlCl3-treated group. Conclusion: Adansonia digitata fruit pulp aqueous extract has a possible benefit in the improvement of AlCl3-memory deficit and AlCl3-induced hippocampal alterations in Wistar rats.

Anahtar Kelimeler

• CA3
• Histology
• Biochemistry
• Neurobehavior
• Phytochemical
• Wistar rats

Neuroprotective Effect of Adansonia digitata against Aluminum Chloride-triggered Memory Deficits and Hippocampal Damage in Rats

Öz

Background: Several reports have shown environmental neuron toxins such as aluminium accumulate in the brain, potentially triggering neurodegenerative disorders. Meanwhile, Adansonia digitata has been shown to possess neuroprotective properties. This study, therefore, assessed the ameliorative properties of Adansonia digitata fruit pulp aqueous extract (AEAD)on aluminum chloride (AlCl3) ¬– induced memory and hippocampal dysfunctions in Wistar rats. The neuroprotective effects were assessed with the Morris water maze for learning and memory, oxidative stress biomarkers glutathione [GSH]), superoxide dismutase [SOD], and (Malondialdehyde [MDA], and histopathological investigation of the CA3 hippocampal region using routine Haematoxylin and Eosin staining techniques. Thirty adult male Wistar rats weighing between 110 and 150 grams were split into six groups at random (n=5). As the Control group, the animals in Group 1 received 2 milliliters per kilogram of distilled water. Group 2 received 100 mg/kg of AlCl3. Ascorbic acid at a dose of 595 mg/kg was given to Group 3. 100 mg/kg AlCl3 and different concentrations of the fruit pulp aqueous extract of Adansonia digitata (500 mg/kg and 1500 mg/kg, respectively) were given to groups 4 and 5. Group 6 received 595 mg/kg of ascorbic acid and 100 mg/kg of AlCl3. Results: The latency time spent to locate the escape platform was observed with remarkable (P<0.05) improvement in the Adansonia digitata fruit pulp aqueous extract treatments compared with the AlCl3-treated group. There was a notable increase in MDA levels and a reduction in SOD and GSH activities in the AlCl3-treated group in relation to the Adansonia digitata fruit pulp aqueous extract-treated groups. Histopathological examination of the CA3 hippocampal region treated with AlCl3 revealed neuronal degenerative changes, whereas, administration of Adansonia digitata fruit pulp aqueous extract ameliorated AlCl3-induced neuronal damages in rats at doses 500mg/kg and 1500mg/kg when compared with the AlCl3-treated group. Conclusion: Adansonia digitata fruit pulp aqueous extract has a possible benefit in the improvement of AlCl3-memory deficit and AlCl3-induced hippocampal alterations in Wistar rats.

Anahtar Kelimeler

• CA3
• Histology
• Biochemistry
• Neurobehavior
• Phytochemical
• Wistar rats

Kaynakça

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