Neuroprotective effects of methyl jasmonate in male Wistar rats exposed to delayed acetic acid-induced ulcerative colitis: involvement of antioxidant status, GFAP, and IBA-1 immunoreactivities.

Autor: Omayone TP; Department of Physiology, School of Basic Medical Sciences, Federal University of Technology, Akure, Ondo State, Nigeria. tpomayone@futa.edu.ng., Salami FT; Department of Physiology, School of Basic Medical Sciences, Federal University of Technology, Akure, Ondo State, Nigeria., Aluko OM; Department of Physiology, School of Basic Medical Sciences, Federal University of Technology, Akure, Ondo State, Nigeria.; The Neuro-Lab, School of Basic Medical Sciences, Federal University of Technology, Akure, Nigeria.; Department of Pharmacology, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria., Nathanniel JN; Department of Physiology, School of Basic Medical Sciences, Federal University of Technology, Akure, Ondo State, Nigeria.; The Neuro-Lab, School of Basic Medical Sciences, Federal University of Technology, Akure, Nigeria., Jeje SO; Department of Physiology, School of Basic Medical Sciences, Federal University of Technology, Akure, Ondo State, Nigeria., Adedeji TG; Department of Physiology, School of Basic Medical Sciences, Federal University of Technology, Akure, Ondo State, Nigeria., Ijomone OM; The Neuro-Lab, School of Basic Medical Sciences, Federal University of Technology, Akure, Nigeria.; Department of Human Anatomy, School of Basic Medical Sciences, Federal University of Technology, Akure, Nigeria.
Jazyk: angličtina
Zdroj: Metabolic brain disease [Metab Brain Dis] 2023 Feb; Vol. 38 (2), pp. 671-686. Date of Electronic Publication: 2023 Jan 03.
DOI: 10.1007/s11011-022-01145-8
Abstrakt: Neurobehavioral deficits have been severally reported as a comorbid outcome in inflammatory bowel diseases (IBDs). This study evaluated neurological changes in the experimental model of IBDs, as well potential protective effects of methyl jasmonate (MJ). The study used the acetic acid model of colitis and thereafter delayed the healing process by the administration of indomethacin (Indo) (2 mg/kg, SC). Thirty male Wistar rats (120-160 g) were divided into 5 groups (n = 6). Control, Colitis, Colitis + Indo, MJ (50 mg/kg, IP) + Colitis and MJ + Colitis + Indo. Colitis was induced by intrarectal administration of 2 mL, 4% acetic acid. Neurobehavioral studies were carried out to assess memory function, depression, and anxiety on day 7 of post-colitis induction. Animals were thereafter sacrificed to collect the brain tissues for routine histology, immunoreactivity of GFAP and IBA-1, and biochemical assays. Neurobehavioral tests showed anxiety, depression, and memory deficits, especially in the Colitis + Indo group which were accompanied by increased IBA-1 and GFAP count. MJ reversed these effects and reduced GFAP count in the hippocampus and amygdala as well as IBA-1 count in the hippocampus, amygdala, and cortex. Histological observations of these areas showed no significant histopathological changes across all groups. GPx and CAT levels were significantly reduced, while MPO was significantly increased in colitis and Colitis+indo groups when compared with control, which was attenuated in groups administered with MJ. These findings tuggest that MJ possesses neuroprotective, anti-oxidant, and neuron-regeneration properties. Therefore, it could be considered as a potential treatment for behavioral deficits associated with ulcerative colitis.
(© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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