Differential protection of black-seed oil on econucleotidase, cholinesterases and aminergic catabolizing enzyme in haloperidol-induced neuronal damage of male rats

黑种草油对氟哌啶醇诱导的雄性大鼠神经元损伤中生态核苷酸酶、胆碱酯酶和胺能分解代谢酶的差异性保护作用

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Abstract

BACKGROUND: The antipsychotic, haloperidol, is extremely efficient in the treatment of schizophrenia but its application is constrained because of irreversible adverse drug reactions. Hence, in this study, we investigate the differential effects of black seed oil on cholinesterase [acetylcholinesterase (AChE) and butrylcholinesterase (BuChE), ectonucleotidase (5'-nucleotidase), lactate dehydrogenase (LDH) and monoamine oxidase (MAO)] activities and relevant markers of oxidative stress in the cerebrum of haloperidol-induced neuronal-damaged rats. METHODS: The animals were divided into six groups (n = 10): normal control rats; haloperidol-induced rats: induced rats were pre-, co- and post-treated with black-seed oil respectively, while the last group was treated with extract oil only. The treatment was performed via oral administration and the experiment lasted 14 days. RESULTS: The results revealed an increase in 5(I) nucleotidase, a marker of adenosine triphosphate (ATP) and adenosine monophosphate (AMP) hydrolysis, as well as AChE, BuChE and MAO activities, with concomitant decrease in LDH activity of cerebrum in induced rats when compared with controls. Also, administration of haloperidol caused systemic oxidative damage and adverse histopathological changes in neuronal cells, indications of mental disorder. The differential treatments with black-seed oil prevented these alterations by increasing LDH and decreasing 5(I) nucleotidase, AChE, BuChE and MAO activities in the cerebrum. Essential oil post-treatment is most efficacious in reversing haloperidol-induced neuronal damage in rat; followed by pre- and cotreatment, respectively. CONCLUSIONS: We concluded that essential black-seed oil enhanced the wellness of aminergic, purinergic and cholinergic neurotransmissions of haloperidol-induced neuronal damage in rats.

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