Neuroprotective effect of Moringa oleifera leaf extract on aluminium-induced temporal cortical degeneration

Abstract

Aluminium (Al), one of the metals implicated in neurodegeneration easily gain access to the nervous system through its presence in many manufactured foods, medicines and drinking water, and causes neurotoxicity utilizing the reactive oxygen specie pathway. The need to curtail these effects on the nervous system motivated the use of the plant Moringa oleifera (MO). This study thus, investigated the neuroprotective effects of MO leaf extract on aluminium-induced temporal cortical degeneration in rats. 24 male albino Wistar rats were grouped (n = 6) into control (1 ml/kg distilled water), l00 mg/kg aluminium chloride (AlCl₃), 300 mg/kg MO, and 100 mg/kg AlCl₃ and 300 mg/kg MO groups. The administration lasted for 28 days and the rats were sacrificed on day 29 by perfusion-fixation after blood was obtained for serum Al estimation. The brain tissues were then routinely processed for some histological and immunnolabelling studies. There was no significant difference in serum Al in the test groups. Histological results showed atrophied and karyorrhetic cells with loss of Nissl substance in the temporal cortex of the AlCl₃ group, while no adverse effect was observed in the cytoarchitecture of the temporal cortex and Nissl substance of the MO group. However, groups which were administered AlCl₃ simultaneously with MO extract showed less degenerative features in the cyto-architecture of the temporal cortex with normal Nissl substance staining. There was increased neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP) expressions in the AlCl₃ group, while the MO group also showed increased NSE but decreased GFAP expression. However, the group which were administered AlCl₃ simultaneously with MO extract showed less expression of NSE and GFAP. In conclusion, MO protects against Al-induced neurotoxicity of the temporal cortex of rats.

Keywords: Aluminium; Immunolabelling; Moringa oleifera; Neurodegeneration; Neuroprotection.