Diosgenin reverses posttraumatic stress disorder in mice by augmenting neurochemical release and inhibiting HPA axis dysfunction, oxidative stress, and neuroinflammation

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dc.contributor.authorBenneth Ben-Azu
dc.contributor.authorOlusegun G. Adebayo
dc.contributor.authorAdaeze Adebesin
dc.contributor.authorKenneth C. Oparaji
dc.contributor.authorVivian O. Ojiakor
dc.contributor.authorGift C. Pender
dc.contributor.authorBensandy O. Odeghe
dc.contributor.authorNoah A. Omeiza
dc.contributor.authorAbdulrahim Halimat A
dc.contributor.authorVivian Ezieshi
dc.contributor.authorGlory Ighosotu
dc.contributor.authorEmmanuel Omo-Odudu
dc.contributor.authorEkene I. Monye
dc.date.accessioned2025-05-09T17:19:26Z
dc.date.available2025-05-09T17:19:26Z
dc.date.issued2024-07
dc.description.abstractPost-traumatic stress disorder (PTSD) is a mental disorder linked to neurochemical, hypothalamic-pituitary- adrenal (HPA)-axis dysregulations, inflammatory and pro-oxidant challenges in response to traumatic events. It is one of the leading causes of neurocognitive declines, hence prompting the need for a pharmacological intervention. However, the impact of diosgenin, a naturally occurring steroidal saponin with adaptogenic-like action, on PTSD-induced neuropsychiatric disturbances and its underlying mechanisms are unknown. In this study, we investigated the outcome of diosgenin treatment in a multimodal traumatic, single prolonged stress (SPS)-induced PTSD in mice. Following the SPS-induced 7 days of PTSD, mice (n = 9) were thereafter treated with diosgenin (25 and 50 mg/kg) or fluoxetine (10 mg/kg) orally from days 8–20 (14 days). Locomotory, cognitive-, depressive- and anxiety-like behaviors were investigated. We assayed for changes in adrenal weight, serum glucose and corticosterone concentrations. Neurochemical, inflammatory, oxido-nitrergic dysfunctions and monoamine oxidase-B and acetylcholinesterase activities, were measured in the striatum, prefrontal-cortex and hippocampus. The results revealed that the SPS challenge inhibited locomotor, spatial/non-spatial memory functions, increased anxiety and depressive-like features, which were reversed by diosgenin. Diosgenin reduced SPS-induced increased monoamine oxidase-B, acetylcholinesterase activities, TNF-α, IL-6, malondialdehyde and nitrite levels in the striatum, prefrontal-cortex and hippocampus. Antioxidants such as glutathione, superoxide- dismutase, and catalase levels in SPS-mice brains were increased by diosgenin. Moreover, diosgenin attenuated SPS-induced hyper-HPA-axis mediation of PTSD by decreasing serum corticosterone, glucose levels and adrenal gland hypertrophy. Herewith, we suggest that diosgenin convenes adaptogenic-like protection against mice exposed to PTSD by enhancing antioxidant machinery, neurochemical modulations, and inhibition of oxido- nitrergic, inflammatory, and HPA-axis dysfunctions.
dc.identifier.citationDiosgenin Neurotransmitters Single prolonged stress Posttraumatic stress disorder Adaptogens
dc.identifier.urihttps://doi.org/10.1016/j.jadr.2024.100814
dc.identifier.urihttps://uilspace.unilorin.edu.ng/handle/123456789/16587
dc.language.isoen
dc.publisherJournal of Affective Disorders Reports
dc.relation.ispartofseriesVolume 17; 1-12
dc.titleDiosgenin reverses posttraumatic stress disorder in mice by augmenting neurochemical release and inhibiting HPA axis dysfunction, oxidative stress, and neuroinflammation
dc.typeArticle

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