Preclinical studies have reported that Murraya koenigiileaves (MKL) could enhance memory. MKL is also known for its antioxidant activity. The current study was to assess the possible neuroprotective potential of MKL methanolic extract in a two vessel occlusion (2VO) rat model of partial global cerebral ischaemia. Methods:Rats were divided into memory and learning groups. Each group was subdivided into sham control, untreated 2VO and MKL-treated 2VO subgroups. The Morris water maze test was implemented to assess the rats’ cognitive function postoperatively. Brain samples were histopathologically examined for viable neurons within the CA1 hippocampal region. Results: Water maze test findings showed that MKL positively improved memory and learning impairments. However, this improvement in memory test for the treated group was still significantly inferior to that of the healthy control group. Additionally, MKL treated group exhibited insignificant difference in the number of viable hippocampal CA1 pyramidal neurons from that of the untreated 2VO group, whereas both MKL treated and untreated 2VO groups showed significantly less viable neurons when compared with the control group. Conclusion: MKL extract modestly improved memory without providing substantial neuroprotective action to the hippocampal neurons in rats with chronic partial global cerebral ischaemia.
Introduction: The oil extract of black cumin seeds Nigella sativa (NSO) demonstrated considerable
preservation of spatial cognitive functions in rats subjected to chronic brain hypoperfusion (CBH). The hippocampal CA1 region pyramidal cells are the earliest neurons suffering neurodegeneration following CBH. Objective: The current study was devoted to assess the protective effects of Nigella sativa (NSO) treatment on CA1 hippocampal pyramidal cells of rats subjected to chronic brain hypoperfusion (CBH) that was achieved through permanent two vessel occlusion (2VO) procedure. Methods: Twenty four rats were equally divided into three groups; sham control, untreated 2VO and NSO treated group (2VO with daily oral NSO treatment. After the 10th postoperative week coronal sections of the hippocampus were collected for histopathological and electron microscopical examinations. Results: The number of viable pyramidal cells within CA1 hippocampal region in sham control and NSO treated groups was significantly higher than that of untreated 2VO group, while the difference was not significant when comparing the viable pyramidal cells number of sham control with NSO treated groups. Furthermore, 2VO group showed marked intracellular ultrastructural distortions that were less pronounced in NSO treated group. Conclusion: NSO displayed a robust potential to protect hippocampal pyramidal cells from CBH induced neurodegeneration putting forward its prospective neuroprotective activity against age related cognitive decline of Alzheimer’s disease and vascular dementia.