THE EFFECT OF NIGELLA SATIVA OIL ON THE FRONTAL CEREBRAL CORTEX AND HIPPOCAMPUS OF ROTENONE INDUCED MODEL OF PARKINSON S DISEASE IN THE ADULT MALE ALBINO RAT: HISTOLOGICAL AND IMMUNOHISTOCHEMICAL STUDY

Abstract

Introduction: Parkinson's disease (PD) is the second most common neurological ailment globally, following Alzheimer's disease. Cognitive decline and dementia are one of the most incapacitating symptoms affecting patients. Nigella sativa oil (NSO) has neuroprotective, antioxidant and anti-inflammatory properties.Aim of the Work: Our study intended to investigate the neurodegenerative alterations that occur in the frontal cortex and hippocampus of a parkinsonian rat model, and to examine the alleviative effect of NSO. This was determined using behavioral, biochemical, histological, immunohistochemical, and morphometric studies.Materials and Methods: Sixty adult male albino rats were organized into six groups; control, NSO (3 mg/kg b.w/day orally for 30 days), rotenone treated (1.5 mg/kg b.w/day subcutaneous for the last 10 days), pre-treated with NSO for 20 days followed by combined rotenone and NSO for the last 10 days, recovery ( 1.5 mg/kg b.w/day subcutaneous for the first 10 days) and post-treated with NSO + rotenone. Behavioral tests; open field test, forced swim test and Y maze test were performed. After scarification of the rats, studies involving biochemistry, histology and immunohistochemistry were conducted on the brain. (b.w mean body weight of the rat) .Results: The frontal cortex and CA1 region of the hippocampus showed severe degenerative changes especially in the recovery group. This was manifested clinically by impairment in the spatial working memory. This was accompanied by increased Bax protein, GFAP, TNF-α, iNOS immuno-expression with a decrease in Ki67 immuno-expression. Administration of NSO either as a protective agent or as a therapeutic agent greatly improved the results.Conclusion: The administration of NSO may protect the risky individuals from catching the disease or at least delay the onset of its occurrence. Also, its administration after establishment of the disease may decrease the rate of the disease progression and delay the development of the cognitive impairment symptoms.