Evaluation of Apoptotic Changes Using BCL-2 on Aluminium Chloride Induced Neurotoxicity Treated with Ethanolic Extract of Carpolobia lutea at Different Doses

Background: Carpolobia luteais a small tree native to West and Central tropical Africa and it is one of the medicinal plants that play a major role in the health care system of developing countries. It belongs to the plant family polygalaceae. Aluminium is a well-established neurotoxicant involved in the etiology of neurodegenerative diseases.

Aim of the Study: This study was aimed at investigating apoptotic changes using Bcl-2 on aluminium chloride induced hippocampal and striatal damages treated with ethanolic extract of C. lutea at different doses.

Materials and Methods: Thirty sixwistar rats weighing 180-200g were used for this study. The animals were randomized into six groups of six rats each. Group A rats received only animal feed and water. Groups B,C,D,E and F were given 100mg/kg bw of aluminium chloride intraperitoneally five times a week for three weeks to induce neurotoxicity.In order to reverse the neurotoxicity, Group C was treated with 10mg/kg bw of donepezil as standard drug for the hippocampus, also Group D was treated with 20mg/kg bw of Levodopa/5mg/kg bw of Carbidopa as standard drug for striatum while group E and F were treated with 200mg/kg and 400mg/kg of Carpolobia lutea respectively for 14 days. Histopathological study was done on the hippocampus and striatum of the rat brain and thereafter hematoxylin and eosin staining were carried out. Evaluation of apoptosis in the hippocampus and striatum were estimated by an immunohistochemical study using Bcl-2 protein expressions.

Results: Our result revealed that 200mg/kg bwof C. lutea showed a reduced expression of Bcl-2 immunoreactivity than the standard drug (10mg/kg donepezil). Therefore, it is assume that 200mg/kg C. lutea may protect the brain from apoptosis in the hippocampus thereby preventing neurodegenerative diseases. The higher dose (400mg/kg bwC.lutea) showed sign of neurotoxicity by having increase Bcl-2 immunoreactivity. In the striatum, we could find out that lower dose of C. lutea (200mg/kg bw) may distort the initiation of apoptosis in the striatum by having a reduced Bcl-2 immunoreactive expression but it is not more potent compared to 20mg/kg levodopa/5mg/kg Carbidopa (standard drug). The higher dose (400mg/kg bw of C. lutea) may be neurotoxic to the striatum.

Conclusion: In conclusion, the lower dose of C. lutea has neuroprotective activity that could have a promising role in ameliorating age-related neurodegeneration or prevent apoptosis in the hippocampus compared to the standard drug (donepezil). In the striatum, the standard drug (20mg/kg Levodopa/5mg/kg Carbidopa) may still protect the brain better against apoptosis than the lower dose of the plant extract.