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Xylopia parviflora (A. Rich.) Benth. ameliorates ketamine-induced positive, negative, and cognitive symptoms of psychosis through down-regulation of neuro-oxidative damage in mice


A. A. Murtala
E. O. Oyinloye
F. A. Oladoja
H. A. Olasore
L. O. Ogunjimi
A. A. Aderinola
A. O. Alabi
O. O. Soyinka
M. S. Fageyinbo
A. S. Faponle
O. O. Shonde
L. E. Osipitan

Abstract

Background: Ethno-botanical investigations on Xylopia parviflora (A. Rich.) Benth. revealed its application in the management of neurological disorders, including psychotic conditions.


Objective: To evaluate the neuroprotective effects of the hydroethanol leaf extract of Xylopia parviflora (XPE) on the positive, negative, and cognitive manifestations of psychosis in mouse models. .


Methods: Thirty mice were allocated into six groups (n=5). Treatments for each group are as follows: distilled water only (10 mL/kg; Grp A), distilled water + ketamine (50 mg/kg; Grp B), the extract (50, 100, and 200 mg/kg; Grps C-E), and haloperidol (5 mg/kg; Grp F). One hour subsequent to the administration of the extract and haloperidol, all groups were administered ketamine (50 mg/kg, i.p.) to induce psychosis. These treatment regimens were repeated over a period of 21 consecutive days. Twenty-four hours following the final treatment, the mice underwent forced swim (FST), open field (OFT), and object recognition tests (ORT), during which relevant parameters were monitored for a duration of five minutes. Thereafter, the animals were euthanized via cervical dislocation, and their brain tissues were harvested for antioxidant analyses.


Results: XPE (50-200 mg/kg) diminished the duration of immobility in the FST; enhanced the duration spent with the novel object and reduced the duration spent with the familiar object in the ORT; and diminished the frequency of section crossings in the OFT when compared with the distilled water + ketamine treated group. Furthermore, XPE increased antioxidant biomarkers in the brain.


Conclusion: XPE ameliorates ketamine-induced symptoms of psychosis through the attenuation of oxidative stress.


Journal Identifiers


eISSN: 2635-3555
print ISSN: 0189-8434