Acute Treatment with Fucoidan Ameliorates Traumatic Brain Injury-Induced Neurological Damages and Memory Deficits in Rats: Role of BBB Integrity, Microglial Activity, Neuroinflammation, and Oxidative Stress.

There is no acquiesced remedy for the treatment of traumatic brain injury (TBI)-associated impairment, especially cognitive decline. The first 24 h after TBI is a golden time for preventing the progress of the impairments. The present study aimed to examine the acute effects of fucoidan on neurological outcomes and memory performance and investigate its potential mechanisms in rats with TBI.

Uncovering the protective potential of vanillic acid against traumatic brain injury-induced cognitive decline in male rats: Insights into underlying mechanisms.

Traumatic brain injury (TBI) is a significant contributor to global mortality and disability, and there is still no specific drug available to treat cognitive deficits in survivors. Vanillic acid (VA), a bioactive phenolic compound, has shown protective effects in various models of neurodegeneration; however, its impact on TBI outcomes remains elusive. Therefore, this study aimed to elucidate the possible role of VA in ameliorating TBI-induced cognitive decline and to reveal the mechanisms involved.

Neuroprotective effects of silymarin in 3-nitropropionic acid-induced neurotoxicity in male mice: improving behavioral deficits by attenuating oxidative stress and neuroinflammation.

3-Nitropropionic acid (3-NP) is strongly believed to be an irreversible inhibitor of mitochondrial complex II, leading to neural damage. This study aimed to investigate the neuroprotective effects of silymarin against 3-NP-induced neurotoxicity in male mice. Six-week-old mice received subacute doses of 3-NP intraperitoneally for 17 days.

Silibinin chronic treatment in a rat model of Parkinson disease: A comprehensive in-vivo evaluation and in silico molecular modeling.

Background: Apoptosis, oxidative stress, and neuroinflammation have been linked to the onset of Parkinson's disease (PD). Although the pre-treatment effects of Silibinin on a PD model have been evaluated, in the current study we investigated the chronic therapeutic effects of Silibinin microinjection on a rat model of established parkinsonism along with behavioral and laboratory markers assessments.

Method: Parkinsonism was induced by 6-hydroxydopamine (6-OHDA, 8 μg/2μl/rat).

Post treatment with Gastrodin suppresses oxidative stress and attenuates motor disorders following 6-OHDA induced Parkinson disease.

Background & Objective: Researchers are currently trying to find new therapies with better symptomatic activity and fewer side effects to manage Parkinson's disease (PD). Although the protective effect of pre-treatment by Gastrodin (Gst) on a PD model has been evaluated, in the current experimental study, we investigated the symptomatic therapeutic effects of Gst microinjection in the same PD model but in the post-parkinsonism induction condition.

Methods: Parkinsonism was induced by unilateral infusion of 6- hydroxydopamine (6-OHDA; 8 μg/ 2 μl/ rat) into the central region of the substantia nigra pars compacta (SNc).

Silymarin and neurodegenerative diseases: Therapeutic potential and basic molecular mechanisms.

Background: Neurodegenerative diseases (NDDs) are primarily characterized by selective neuronal loss in the brain. Alzheimer's disease as the most common NDDs and the most prevalent cause of dementia is characterized by Amyloid-beta deposition, which leads to cognitive and memory impairment. Parkinson's disease is a progressive neurodegenerative disease characterized by the dramatic death of dopaminergic neuronal cells, especially in the SNc and caused alpha-synuclein accumulation in the neurons.

Neuronal degeneration and oxidative stress in the SNc of 6-OHDA intoxicated rats; improving role of silymarin long-term treatment.

Progressive loss in dopaminergic neurons (DA) of substantia nigra pars compacta (SNc) leads to Parkinson's disease with a hypothesis of oxidative stress generation. The present study was conducted to determine the long-term efficacy of silymarin (SM) post-treatment on 6-OHDA-induced oxidative stress in the SNc of male rats. Male Wistar rats were received 6-OHDA (8 μg/rat) into SNc.

Silymarin prevents apoptosis through inhibiting the Bax/caspase-3 expression and suppresses toll like receptor-4 pathway in the SNc of 6-OHDA intoxicated rats.

Background And Purpose: Several lines of evidence show that apoptosis, oxidative stress and neuroinflammation are associated with the development of Parkinson's disease (PD). In the present study, we investigated the effect of pre-treatment with silymarin (SM) on oxidative stress, apoptosis and toll-like receptor 4 (TLR4) expression in substantia nigra pars copmacta (SNc) of 6-hydroxydopamine (6-OHDA)-lesioned rats.

Methods: Animals were pretreated with 100, 200 or 300 mg/kg of SM daily for 5 days and at 6th day 6-OHDA (8 μg/2 μl) was infused unilaterally into the central region of the SNc.

Short-Term Treatment with Silymarin Improved 6-OHDA-Induced Catalepsy and Motor Imbalance in Hemi-Parkisonian Rats.

Purpose: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by disabling motor abnormalities, which include tremor, muscle stiffness, paucity of voluntary movements, and postural instability. Silymarin (SM) or milk thistle extract, is known to own antioxidative, anti-apoptotic, anti-inflammatory and neuroprotective effects. In the present study, we investigated the effect of intraperitoneal (i.

Silymarin improved 6-OHDA-induced motor impairment in hemi-parkisonian rats: behavioral and molecular study.

Background: Neuroinflammation and oxidative stress has been shown to be associated with the development of Parkinson disease (PD). In the present study, we investigated the effect of intraperitoneal (i.p.

Pre-treatment with silymarin reduces brain myeloperoxidase activity and inflammatory cytokines in 6-OHDA hemi-parkinsonian rats.

Most chronic neurodegenerative diseases such as Parkinson's disease (PD) are accompanied by neuroinflammation which is associated with glial cells activation and production of different inflammatory cytokines. In the present study we evaluated the anti-cataleptic effect of silymarin pre-treatment in 6-hydroxydopamine (6-OHDA)-lesioned rats, striatum myeloperoxidase (MPO) activity and cerebrospinal fluid (CSF) levels of inflammatory cytokines. Male Wistar rats were pre-treated with intraperitoneal (i.