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Neuroprotective, antioxidant, anti-inflammatory, and neuromodulatory effects of Calliandra portoricensis root bark ethanol extract against carbon tetrachloride-induced neurotoxicity in male Wistar rats

Bibliographic Data

ID24214633
AuthorsSiemuri Ogugu Ese (0000-0002-6883-7259), Abdulganiu Adedayo Balqees, Ajagbe Maruf Ola (0009-0004-8376-8425), Abegunde Folorunso Joshua, Ibikunle Olufemi Margaret, Achem Jonah
Year2027
Volume374
IssuePt 1
Pages122449
Publication date2027-02-01
Open AccessYes
TypeARTICLE
VenueJournal of Ethnopharmacology (JOURNAL)
Journal identifiersISSN: 0378-8741 • E-ISSN: 1872-7573
PublisherElsevier BV (PUBLISHER)
DOI10.1016/j.jep.2026.122449
PMID42810462
OpenAlexW7214771598
LanguageEN
References cited68

Ethnopharmacological relevance Calliandra portoricensis (Jacq.) Benth. is used in the ethnomedicine of southwestern Nigeria in treating epilepsy, convulsion, pain, inflammatory disorders, fever and other neurological conditions. However, its neuroprotective potential has not been adequately investigated. Aim of the study This study evaluated the neuroprotective, antioxidant, anti-inflammatory, and neuromodulatory effects of Calliandra portoricensis root bark ethanol extract (CPRBEE) against carbon tetrachloride (CCl 4 )-induced neurotoxicity in male Wistar rats. Materials and methods CPRBEE was characterized using phytochemical screening and gas chromatography–mass spectrometry (GC–MS). Thirty-five male Wistar rats were randomly allotted to seven groups (n = 5). Neurotoxicity was induced with CCl 4 (1.3 mL/kg; 3:10 v/v in olive oil). Following induction, rats received vitamin C (200 mg/kg) or CPRBEE (10, 20, 30, and 40 mg/kg). Neurobehavioral performance, oxidative stress biomarkers, acetylcholinesterase activity, inflammatory cytokines, neuronal injury markers, trace metal concentrations, Nrf2, HO-1, NF-κB, BDNF concentrations, and histopathological changes were evaluated. Results GC–MS analysis tentatively annotated several phytochemicals, including phytol, β-sitosterol, stigmasterol, squalene, and a vitamin E (tocopherol derivative) peak consistent with α-tocopherol. CCl 4 exposure significantly increased lipid peroxidation, acetylcholinesterase activity, pro-inflammatory cytokines, NSE, GFAP, and NF-κB concentrations, while reducing antioxidant defenses, Nrf2, HO-1, and BDNF concentrations (p < 0.05). CPRBEE attenuated these alterations, improved behavioural performance, partially restored trace-element profiles, and reduced histopathological alterations, with the magnitude of effects varying across biomarkers and treatment levels. Conclusion CPRBEE demonstrated neuroprotective activity against CCl 4 -induced neurotoxicity, potentially through attenuation of oxidative stress and inflammation while preserving antioxidant and neurotrophic defenses, supporting its traditional applications.

Acetylcholinesterase · anti-inflammatory activity · Brain-derived neurotrophic factor · heme oxygenase-1 · inflammatory cytokines · Lipid peroxidation · neurobehavioral performance · Neuromodulation · Neuroprotection · NF-κB · Nrf2 · Oxidative stress · phytochemicals · trace elements · Traditional medicine · Medicinal Plant Research · Medicinal Plants and Neuroprotection · Phytochemistry Medicinal Plant Applications

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Highly citedNo

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