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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

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Abstract

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.

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The data for this study are available from the corresponding author on reasonable request.

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Acknowledgments

OMI acknowledges the support of the International Brain Research Organization (IBRO) and the International Society for Neurochemistry (ISN). Authors acknowledge the technical support of Ms. Joy Iroegbu, of The Neuro- Lab, Mr. Seyi Olabanji Aleruwa and Mr. Ismail Akanni Oguntade (technologist at the Department of Physiology), School of Basic Medical Sciences, Federal University of Technology, Akure, Nigeria.

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Contributions

All authors contributed to the study conception and design. Authors TPO, OMA, FTS and JNN were involved in material preparation and data collection. OMI performed histology and immunohistochemistry assays. All authors were involved in data analysis. Faizah Tobi Salami wrote the first draft of the manuscript and all authors made corrections. All authors read and approved the final manuscript.

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Correspondence to Tosan P. Omayone.

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Animals were handled according to the Guide for the Care and Use of Laboratory Animals by the National Research Council (US), 2011. The experiments were approved by the Ethics Committee of the University of Ibadan and given the number UI-ACUREC/App/2016/034.

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The authors have no relevant financial or non-financial interests to disclose.

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Omayone, T.P., Salami, F.T., Aluko, O.M. et al. 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. Metab Brain Dis 38, 671–686 (2023). https://doi.org/10.1007/s11011-022-01145-8

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  • DOI: https://doi.org/10.1007/s11011-022-01145-8

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