Neuroscience, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Neuroscience, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Psychopharmacology, Journal Year: 2024, Volume and Issue: 241(4), P. 785 - 803
Published: Feb. 5, 2024
Language: Английский
Citations
17IBRO Neuroscience Reports, Journal Year: 2024, Volume and Issue: 16, P. 86 - 97
Published: Jan. 3, 2024
A decrease in the levels of antioxidant arsenals exacerbate generation reactive oxygen/nitrogen species, leading to neurochemical dysfunction, with significant impact on pathogenesis psychotic disorders such as schizophrenia. This study examined preventive and reversal effects diosgenin, a phyto-steroidal saponin functions mice treated ketamine which closely replicates schizophrenia-like symptoms human laboratory animals. In phase, adult cohorts were clustered into 5 groups (n = 9). Groups 1 2 received saline (10 mL/kg, i.p.), 3 4 pretreated diosgenin (25 50 mg/kg), group risperidone (0.5 mg/kg) orally for 14 days. Mice 2-5 additionally daily dose (20 mg/kg, i.p.) or mL/kg/day, i.p.). intraperitoneal injection consecutive days prior mg/kg/p.o./day) treatment from 8-14. assessed behavioral changes. Oxidative, nitrergic markers, cholinergic (acetylcholinesterase activity) transmission striatum, prefrontal-cortex hippocampus. Diosgenin prevented reversed hyperlocomotion, cognitive social deficits relative groups. The increased acetylcholinesterase, malondialdehyde nitrite produced by reduced hippocampus, but did not reverse striatal level. glutathione, catalase levels, except hippocampal activity when compared controls. Conclusively, these biochemical changes might be related ketamine-treated mice, diosgenin.
Language: Английский
Citations
14Neurochemistry International, Journal Year: 2024, Volume and Issue: 177, P. 105748 - 105748
Published: May 3, 2024
Language: Английский
Citations
11Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15
Published: Feb. 26, 2024
Ginsenoside Rg3, a compound derived from
Language: Английский
Citations
9Brain Disorders, Journal Year: 2025, Volume and Issue: unknown, P. 100210 - 100210
Published: March 1, 2025
Language: Английский
Citations
1Journal of Psychiatric Research, Journal Year: 2023, Volume and Issue: 168, P. 165 - 175
Published: Oct. 27, 2023
Language: Английский
Citations
22Journal of Affective Disorders Reports, Journal Year: 2024, Volume and Issue: 17, P. 100814 - 100814
Published: June 26, 2024
Post-traumatic stress disorder (PTSD) is a mental linked to neurochemical, hypothalamic-pituitary-adrenal (HPA)-axis dysregulations, inflammatory and pro-oxidant challenges in response traumatic events. It one of the leading causes neurocognitive declines, hence prompting need for pharmacological intervention. However, impact diosgenin, naturally occurring steroidal saponin with adaptogenic-like action, on PTSD-induced neuropsychiatric disturbances its underlying mechanisms are unknown. In this study, we investigated outcome diosgenin treatment multimodal traumatic, single prolonged (SPS)-induced PTSD mice. Following SPS-induced 7 days PTSD, mice (n = 9) were thereafter treated (25 50 mg/kg) or fluoxetine (10 orally from 8–20 (14 days). Locomotory, cognitive-, depressive- anxiety-like behaviors investigated. We assayed changes adrenal weight, serum glucose corticosterone concentrations. Neurochemical, inflammatory, oxido-nitrergic dysfunctions monoamine oxidase-B acetylcholinesterase activities, measured striatum, prefrontal-cortex hippocampus. The results revealed that SPS challenge inhibited locomotor, spatial/non-spatial memory functions, increased anxiety depressive-like features, which reversed by diosgenin. Diosgenin reduced oxidase-B, TNF-α, IL-6, malondialdehyde nitrite levels Antioxidants such as glutathione, superoxide-dismutase, catalase SPS-mice brains Moreover, attenuated hyper-HPA-axis mediation decreasing corticosterone, gland hypertrophy. Herewith, suggest convenes protection against exposed enhancing antioxidant machinery, neurochemical modulations, inhibition oxido-nitrergic, HPA-axis dysfunctions.
Language: Английский
Citations
7Journal of Psychiatric Research, Journal Year: 2024, Volume and Issue: 179, P. 141 - 155
Published: Sept. 13, 2024
Language: Английский
Citations
7Neurochemical Research, Journal Year: 2022, Volume and Issue: 48(3), P. 816 - 829
Published: Nov. 9, 2022
Language: Английский
Citations
23Frontiers in Cellular Neuroscience, Journal Year: 2023, Volume and Issue: 17
Published: May 15, 2023
Brain aging, which involves a progressive loss of neuronal functions, has been reported to be premature in probands affected by schizophrenia (SCZ). Evidence shows that SCZ and accelerated aging are linked changes epigenetic clocks. Recent cross-sectional magnetic resonance imaging analyses have uncovered reduced brain reserves connectivity patients with compared typically individuals. These data may indicate early abnormalities function following cyto-architectural alterations SCZ. The current mechanistic knowledge on changes, their neuropsychiatric disease association remains incomplete. With this review, we explore summarize evidence the dynamics gut-resident bacteria can modulate molecular contribute age-related neurodegenerative disorders. It is known environmental factors such as mode birth, dietary habits, stress, pollution, infections microbiota system regulate intrinsic activity through vagus nerve enteric nervous system. Microbiota-derived molecules trigger continuous activation microglial sensome, groups receptors proteins permit microglia remodel neurochemistry based complex activities. This remodeling causes aberrant plasticity fetal developmental stages, after onset first-episode psychosis. In central system, microglia, resident immune surveillance cells, involved neurogenesis, phagocytosis synapses neurological dysfunction. Here, review recent emerging experimental clinical regarding gut-brain axis involvement pathology etiology, hypothesis reserve induced infections, other factors. We also include our possibilities consequences gut dysbiosis activities dysfunction, together effects antipsychotics microbiome: therapeutic adverse effects, role fecal transplant psychobiotics sensomes, SCZ-derived aging. end suggestions applicable setting. For example, propose might antipsychotic-induced benefits or well reduce process axis. Overall, hope will help increase understanding pathogenesis related chronobiology microbiome, reveal new concepts serve novel treatment targets for
Language: Английский
Citations
15