stilbenes and Brain-Injuries--Traumatic

stilbenes has been researched along with Brain-Injuries--Traumatic* in 14 studies

Reviews

2 review(s) available for stilbenes and Brain-Injuries--Traumatic

ArticleYear
Inflammation in Fibrodysplasia Ossificans Progressiva and Other Forms of Heterotopic Ossification.
    Current osteoporosis reports, 2019, Volume: 17, Issue:6

    Heterotopic ossification (HO) is associated with inflammation. The goal of this review is to examine recent findings on the roles of inflammation and the immune system in HO. We examine how inflammation changes in fibrodysplasia ossificans progressiva, in traumatic HO, and in other clinical conditions of HO. We also discuss how inflammation may be a target for treating HO.. Both genetic and acquired forms of HO show similarities in their inflammatory cell types and signaling pathways. These include macrophages, mast cells, and adaptive immune cells, along with hypoxia signaling pathways, mesenchymal stem cell differentiation signaling pathways, vascular signaling pathways, and inflammatory cytokines. Because there are common inflammatory mediators across various types of HO, these mediators may serve as common targets for blocking HO. Future research may focus on identifying new inflammatory targets and testing combinatorial therapies based on these results.

    Topics: Adaptive Immunity; Animals; Anti-Inflammatory Agents, Non-Steroidal; Arthroplasty, Replacement, Hip; Blast Injuries; Brain Injuries, Traumatic; Burns; Cell Differentiation; Cytokines; Humans; Hypoxia; Immunosuppressive Agents; Inflammation; Janus Kinase Inhibitors; Macrophages; Mast Cells; Mesenchymal Stem Cells; Myositis Ossificans; Ossification, Heterotopic; Postoperative Complications; Pyrazoles; Receptors, Retinoic Acid; Retinoic Acid Receptor gamma; Signal Transduction; Sirolimus; Spinal Cord Injuries; Stilbenes; Wounds and Injuries

2019
Inhibition of Glycogen Synthase Kinase-3: An Emerging Target in the Treatment of Traumatic Brain Injury.
    Journal of neurotrauma, 2016, 12-01, Volume: 33, Issue:23

    Although traumatic brain injury (TBI) has been a major public health concern for decades, the pathophysiological mechanism of TBI is not clearly understood, and an effective medical treatment of TBI is not available at present. Of particular concern is sustained TBI, which has a strong tendency to take a deteriorating neurodegenerative course into chronic traumatic encephalopathy (CTE) and dementia, including Alzheimer's disease. Tauopathy and beta amyloid (Aβ) plaques are known to be the key pathological markers of TBI, which contribute to the progressive deterioration associated with TBI such as CTE and Alzheimer's disease. The multiple lines of evidence strongly suggest that the inhibition of glycogen synthase kinase-3 (GSK-3) is a potential target in the treatment of TBI. GSK-3 constitutively inhibits neuroprotective processes and promotes apoptosis. After TBI, GSK-3 is inhibited through the receptor tyrosine kinase (RTK) and canonical Wnt signaling pathways as an innate neuroprotective mechanism against TBI. GSK-3 inhibition via GSK-3 inhibitors and drugs activating RTK or Wnt signaling is likely to reinforce the innate neuroprotective mechanism. GSK-3 inhibition studies using rodent TBI models demonstrate that GSK-3 inhibition produces diverse neuroprotective actions such as reducing the size of the traumatic injury, tauopathy, Aβ accumulation, and neuronal death, by releasing and activating neuroprotective substrates from GSK-3 inhibition. These effects are correlated with reduced TBI-induced behavioral and cognitive symptoms. Here, we review studies on the therapeutic effects of GSK-3 inhibition in TBI rodent models, and critically discuss the issues that these studies address.

    Topics: Animals; Brain Injuries, Traumatic; Drug Delivery Systems; Enzyme Inhibitors; Glycogen Synthase Kinase 3; Humans; Neuroprotective Agents; Resveratrol; Stilbenes; Treatment Outcome

2016

Other Studies

12 other study(ies) available for stilbenes and Brain-Injuries--Traumatic

ArticleYear
2, 3, 5, 4'-tetrahydroxystilbene-2-O-beta-D-glucoside protects against neuronal cell death and traumatic brain injury-induced pathophysiology.
    Aging, 2022, 03-21, Volume: 14, Issue:6

    Traumatic brain injury (TBI) is a global health issue that affects at least 10 million people per year. Neuronal cell death and brain injury after TBI, including apoptosis, inflammation, and excitotoxicity, have led to detrimental effects in TBI. 2, 3, 5, 4'-tetrahydroxystilbene-2-O-beta-D-glucoside (THSG), a water-soluble compound extracted from the Chinese herb Polygonum multiflorum, has been shown to exert various biological functions. However, the effects of THSG on TBI is still poorly understood. THSG reduced L-glutamate-induced DNA fragmentation and protected glial and neuronal cell death after L-glutamate stimulation. Our results also showed that TBI caused significant behavioral deficits in the performance of beam walking, mNSS, and Morris water maze tasks in a mouse model. Importantly, daily administration of THSG (60 mg/kg/day) after TBI for 21 days attenuated the injury severity score, promoted motor coordination, and improved cognitive performance post-TBI. Moreover, administration of THSG also dramatically decreased the brain lesion volume. THSG reduced TBI-induced neuronal apoptosis in the brain cortex 24 h after TBI. Furthermore, THSG increased the number of immature neurons in the subgranular zone (SGZ) of the dentate gyrus (DG) of the hippocampus. Our results demonstrate that THSG exerts neuroprotective effects on glutamate-induced excitotoxicity and glial and neuronal cell death. The present study also demonstrated that THSG effectively protects against TBI-associated motor and cognitive impairment, at least in part, by inhibiting TBI-induced apoptosis and promoting neurogenesis.

    Topics: Animals; Apoptosis; Brain Injuries, Traumatic; Glucosides; Hippocampus; Humans; Mice; Stilbenes

2022
Resveratrol activates the SIRT1/PGC-1 pathway in mice to improve synaptic-related cognitive impairment after TBI.
    Brain research, 2022, 12-01, Volume: 1796

    Traumatic brain injury (TBI) is the most common form of craniocerebral injury. Post-TBI neurological impairment is often accompanied by cognitive dysfunction. The potential molecular mechanisms of post-TBI cognitive impairment are not well characterized. Resveratrol, a natural polyphenolic agent, has been shown to improve cognitive function in neurological disorders and aging models through its anti-inflammatory activity. However, whether it can affect synapses to improve cognitive function and the potential mechanisms are not clear. Synapse plays an important role in cognitive function, and synaptophysin(SYN) is one of the important factors involved in synapse formation. Sirtuin 1 (SIRT1) has a neuroprotective effect via its effect on various biological processes, such as inflammation, metabolism, apoptosis, and autophagy. The results of this research suggest that resveratrol increases synaptophysin by activating the SIRT1/PGC-1 pathway and improves post-TBI cognitive function. Use of SIRT1 inhibitor (EX-527) and agonist (SRT1720) in the mice experiments verified the effect and mechanism of action of resveratrol in improving cognitive function. Our study identifies potential therapeutic targets for post-TBI cognitive dysfunction.

    Topics: Animals; Brain Injuries, Traumatic; Cognitive Dysfunction; Mice; Neuroprotective Agents; Peroxisome Proliferator-Activated Receptors; Resveratrol; Sirtuin 1; Stilbenes; Synaptophysin

2022
Polydatin alleviates traumatic brain injury: Role of inhibiting ferroptosis.
    Biochemical and biophysical research communications, 2021, 06-04, Volume: 556

    Secondary injury is the main cause of high mortality and poor prognosis of TBI, which has recently been suggested to be related to ferroptosis. Polydatin, a monocrystalline compound extracted from the rhizome of Polygonum, has been shown to exert potential neuroprotective effects. However, its role and mechanism in the secondary injury of TBI has not been elucidated. In this study, the inhibition of Polydatin on ferroptosis was observed both in the hemoglobin treated Neuro2A cells in vitro and in TBI mouse model in vivo, characterized by reversion of accumulation or deposition of free Fe

    Topics: Animals; Brain; Brain Injuries, Traumatic; Cell Line; Cell Survival; Disease Models, Animal; Ferroptosis; Glucosides; Hemin; Iron; Male; Mice; Mice, Inbred C57BL; Neurons; Neuroprotection; Neuroprotective Agents; Phospholipid Hydroperoxide Glutathione Peroxidase; Stilbenes

2021
Polydatin alleviates severe traumatic brain injury induced acute lung injury by inhibiting S100B mediated NETs formation.
    International immunopharmacology, 2021, Volume: 98

    Severe traumatic brain injury (sTBI)-induced acute lung injury (sTBI-ALI) is regarded as the most common complication of sTBI that is an independent predictor of poor outcomes in patients with sTBI and strongly increases sTBI mortality. Polydatin (PD) has been shown to have a potential therapeutic effect on sTBI-induced neurons injury and sepsis-induced acute lung injury (ALI), therefore, it is reasonable to believe that PD has a protective effect on sTBI-ALI. Here, to clarify the PD protective effect following sTBI-ALI, a rat brain injury model of lateral fluid percussion was established to mimic sTBI. As a result, sTBI induced ALI, and caused an increasing of wet/dry weight ratio and lung vascular permeability, as well as sTBI promoted oxidative stress response in the lung; sTBI caused inflammatory cytokines release, such as IL-6, IL-1β, TNF-α and MCP-1; and sTBI promoted NETs formation, mainly including an increasing expression of MPO, NE and CitH3. Simultaneously, sTBI induced a significant increase in the level of S100B; however, when inhibition of S100B, the expression of MPO, NE and CITH3 were significantly inhibited following sTBI. Inhibition of S100B also promoted lung vascular permeability recovery and alleviated oxidative stress response. Furthermore, PD treatmentreduced the pathological lung damage, promoted lung vascular permeability recovery, alleviated oxidative stress response and inflammatory cytokines release; more importantly, PD inhibited the expression of S100B, and NETs formation in the lung following sTBI. These results indicate that PD alleviates sTBI-ALI by inhibiting S100B mediated NETs formation. Thus, PD may be valuable in sTBI-ALI treatment.

    Topics: Acute Lung Injury; Animals; Brain Injuries, Traumatic; Disease Models, Animal; Extracellular Traps; Glucosides; Humans; Lung; Male; Oxidative Stress; Rats; S100 Calcium Binding Protein beta Subunit; Stilbenes

2021
PARP1 might enhance the therapeutic effect of tetrahydroxystilbene glucoside in traumatic brain injury via inhibition of Ras/JNK signalling pathway.
    Folia neuropathologica, 2020, Volume: 58, Issue:1

    Trauma is the main cause of death for people aged 1-45, and among them, traumatic brain injury (TBI) is the major condition, which causes over 50,000 deaths each year and costs over 80 billion per year. Tetrahydroxystilbene glucoside (TSG) is the active ingredient of polygonum multiflorum, a traditional Chinese herbal medicine, which presented multiple pharmacological effects, including antioxidative, anti-inflammatory, reducing blood fat and neuroprotection effects. However, the effect of TSG in promoting the recovery of the nerve system after TBI is not fully understood. PARP1 is a key enzyme in repair of the damage in DNA, which is activated by binding to DNA breaks, initiating both single-strand and double-strand DNA break repair. And we thought that overexpression of TSG might enhance the effect of TSG in TBI treatment. In this study, we firstly detected the oxidative stress response related molecules in serum samples of TBI patients and a TBI mice model, and found that oxidative stress response was activated after TBI, and TSG would reduce this effect. We further noticed that inflammation related molecules presented a similar trend with oxidative stress response related molecules. These results indicated that inflammatory response and oxidative stress processes were both activated after TBI, and reduced after TSG treatment. We further detected that the apoptosis related proteins and anti-oxidative proteins were increased after TSG treatment, and these effects were enlarged after overexpression of PARP1. We further noticed that these effects might be mediated by inhibition of the Ras/JNK signalling pathway. Thus, we thought overexpression of PARP1 might enhance the therapeutic effect of TSG in TBI treatment.

    Topics: Adult; Animals; Brain Injuries, Traumatic; Glucosides; Humans; Male; MAP Kinase Signaling System; Mice; Mice, Inbred C57BL; Middle Aged; Oxidative Stress; Poly (ADP-Ribose) Polymerase-1; ras Proteins; Reactive Oxygen Species; Stilbenes

2020
Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1.
    Molecular medicine reports, 2018, Volume: 17, Issue:2

    The inflammatory response in the cerebral cortex serves an important role in the progression of secondary injury following traumatic brain injury (TBI). The NLR family pyrin domain containing 3 (NLRP3) inflammasome is necessary for initiating inflammation and is involved in various central nervous system disorders. The aim of the present study was to investigate the neuroprotective effect of resveratrol and elucidate the underlying mechanisms of resveratrol associated regulation of the NLRP3 inflammasome in TBI. The results demonstrated that the activation of NLRP3, caspase‑1 and sirtuin 1 (SIRT1), enhanced the production of inflammatory cytokines and reactive oxygen species (ROS) following TBI. Administration of resveratrol alleviated the degree of TBI, as evidenced by the reduced neuron‑specific enolase (NSE) and brain water content (WBC). Resveratrol pretreatment also inhibited the activation of NLRP3 and caspase‑1, and reduced the production of inflammatory cytokines and ROS. In addition, resveratrol further promoted SIRT1 activation. Furthermore, the suppressing effect of resveratrol on the NLRP3 inflammasome and ROS was blocked by the SIRT1 inhibitor, sirtinol. The results revealed that the activation of the NLRP3 inflammasome and the subsequent inflammatory responses in the cerebral cortex were involved in the process of TBI. Resveratrol may attenuate the inflammatory response and relieve TBI by reducing ROS production and inhibiting NLRP3 activation. The effect of resveratrol on NLRP3 inflammasome and ROS may also be SIRT1 dependent.

    Topics: Animals; Benzamides; Brain Injuries, Traumatic; Caspase 1; Cerebral Cortex; Cytokines; Glutathione; Inflammasomes; Male; Malondialdehyde; Naphthols; Neuroprotective Agents; NLR Family, Pyrin Domain-Containing 3 Protein; Phosphopyruvate Hydratase; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Resveratrol; Sirtuin 1; Stilbenes; Superoxide Dismutase

2018
Resveratrol Attenuates Cognitive Deficits of Traumatic Brain Injury by Activating p38 Signaling in the Brain.
    Medical science monitor : international medical journal of experimental and clinical research, 2018, Feb-22, Volume: 24

    BACKGROUND Traumatic brain injury (TBI) is characterized by cognitive deficits, which was associated with brain oxidative stress and apoptosis. Resveratrol (RSV) is an anti-apoptotic and anti-oxidative. This study aimed to investigate neuroprotective effects and involved molecular mechanisms in TBI. MATERIAL AND METHODS RSV and p38 inhibitor were administrated to TBI rats. Cognitive deficits were evaluated by Morris water maze assay. Reactive oxygen species (ROS) and apoptosis were detected in rat brains by fluorescent staining. Western blotting was used to assess the phosphorylation of p38 and the expression levels of Nrf2, HO1, and activated caspase-3. RESULTS RSV administration attenuated cognitive deficits of TBI rats. The ROS generation and apoptosis in the brain of TBI rats were suppressed by RSV treatment. Moreover, RSV treatment recovered activation of p38/Nrf2/HO1 signaling pathway. The co-administration of p38 inhibitor impaired RSV's attenuating effects on cognitive deficits, brain apoptosis, and ROS generation. CONCLUSIONS RSV attenuated cognitive deficits of TBI by inhibiting oxidative stress-mediated apoptosis via targeting p38/Nrf2 signaling.

    Topics: Animals; Antioxidants; Apoptosis; Brain; Brain Injuries, Traumatic; Cognition; Cognitive Dysfunction; Female; Male; MAP Kinase Signaling System; Neuroprotective Agents; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Resveratrol; Stilbenes

2018
Assessment of a nutritional supplement containing resveratrol, prebiotic fiber, and omega-3 fatty acids for the prevention and treatment of mild traumatic brain injury in rats.
    Neuroscience, 2017, Dec-04, Volume: 365

    Children and adolescents have the highest rates of traumatic brain injury (TBI), with mild TBI (mTBI) accounting for most of these injuries. Adolescents are particularly vulnerable and often suffer from post-injury symptomologies that may persist for months. We hypothesized that the combination of resveratrol (RES), prebiotic fiber (PBF), and omega-3 fatty acids (docosahexaenoic acid (DHA)) would be an effective therapeutic supplement for the mitigation of mTBI outcomes in the developing brain. Adolescent male and female Sprague-Dawley rats were randomly assigned to the supplement (3S) or control condition, which was followed by a mTBI or sham insult. A behavioral test battery designed to examine symptomologies commonly associated with mTBI was administered. Following the test battery, tissue was collected from the prefrontal cortex (PFC) and primary auditory cortex for Golgi-Cox analysis of spine density, and for changes in expression of 6 genes (Aqp4, Gfap, Igf1, Nfl, Sirt1, and Tau). 3S treatment altered the behavioral performance of sham animals indicating that dietary manipulations modify premorbid characteristics. 3S treatment prevented injury-related deficits in the longer-term behavior measures, medial prefrontal cortex (mPFC) spine density, and levels of Aqp4, Gfap, Igf1, Nfl, and Sirt1 expression in the PFC. Although not fully protective, treatment with the supplement significantly improved post-mTBI function and warrants further investigation.

    Topics: Animals; Animals, Newborn; Brain; Brain Injuries, Traumatic; Dietary Supplements; Disease Models, Animal; Exploratory Behavior; Fatty Acids, Omega-3; Female; Gene Expression Regulation; Male; Maze Learning; Memory, Short-Term; Neurofibromatosis 1; Prebiotics; Psychomotor Performance; Rats; Rats, Sprague-Dawley; Resveratrol; Stilbenes; Swimming

2017
Resveratrol Treatment Prevents Hippocampal Neurodegeneration in a Rodent Model of Traumatic Brain Injury.
    Turkish neurosurgery, 2017, Volume: 27, Issue:6

    Traumatic brain injury (TBI) is a complex process. Increasing evidence has demonstrated that reactive oxygen species contribute to brain injury. Resveratrol (RVT) which exhibits significant antioxidant properties, is neuroprotective against excitotoxicity, ischemia, and hypoxia. The aim of this study was to evaluate the neuroprotective effects of RVT on the hippocampus of a rat model of TBI.. Twenty eight rats were divided into four groups. A moderate degree of head trauma was induced using Feeney"s falling weight technique. Group 1 (control) underwent no intervention or treatment. Head trauma was induced in Group 2 (trauma) and no drug was administered. Head trauma was induced in Group 3 and low-dose RVT (50 mg/kg per day) was injected. In Group 4, high-dose RVT (100 mg/kg per day) was used after head trauma. Brain tissues were extracted immediately after perfusion without damaging the tissues. Histopathological and biochemistry parameters were studied.. Brain tissue malondialdehyde (MDA) levels in the trauma group were significantly higher than those in the control, lowdose RVT-treated, and high-dose-RVT-treated groups. The superoxide dismutase (SOD) levels in the control group were significantly higher than those in the trauma, low-dose RVT-treated, and high-dose RVT-treated groups. Glutathione peroxidase (GSH-Px) levels in the control group were significantly higher than those in the trauma and low-dose RVT-treated groups. The level of oxidative deoxyribonucleic acid (DNA) damage (8-OHdG/106 dG) in the trauma group was higher than that in the control group, low-dose RVT-treated, and high-dose RVT-treated groups.. Resveratrol has a healing effect on neurons after TBI.

    Topics: Animals; Antioxidants; Brain Injuries, Traumatic; DNA Damage; Glutathione Peroxidase; Hippocampus; Male; Malondialdehyde; Nerve Degeneration; Neuroprotective Agents; Rats; Resveratrol; Stilbenes; Superoxide Dismutase

2017
Protective effect of resveratrol against nigrostriatal pathway injury in striatum via JNK pathway.
    Brain research, 2017, Jan-01, Volume: 1654, Issue:Pt A

    Nigrostriatal pathway injury is one of the traumatic brain injury models that usually lead to neurological dysfunction or neuron necrosis. Resveratrol-induced benefits have recently been demonstrated in several models of neuronal degeneration diseases. However, the protective properties of resveratrol against neurodegeneration have not been explored definitely. Thus, we employ the nigrostriatal pathway injury model to mimic the insults on the brain. Resveratrol decreased the p-ERK expression and increased the p-JNK expression compared to the DMSO group, but not alter the p38 MAPK proteins around the lesion site by Western blot. Prior to the injury, mice were infused with resveratrol intracerebroventricularly with or without JNK-IN-8, a specific c-JNK pathway inhibitor for JNK1, JNK2 and JNK4. The study assessed modified improved neurological function score (mNSS) and beam/walking test, the level of inflammatory cytokines IL-1β, IL-6 and TNF-α, and striatal expression of Bax and Bcl-2 proteins associated with neuronal apoptosis. The results revealed that resveratrol exerted a neuroprotective effect as shown by the improved mNSS and beam latency, anti-inflammatory effects as indicated by the decreased level of IL-1β, TNF-α and IL-6. Furthermore, resveratrol up-regulated the protein expression of p-JNK and Bcl-2, down-regulated the expression of Bax and the number of Fluoro-Jade C (FJC) positive neurons. However, these advantages of resveratrol were abolished by JNK-IN-8 treatment. Overall, we demonstrated that resveratrol treatment attenuates the nigrostriatal pathway injury-induced neuronal apoptosis and inflammation via activation of c-JNK signaling.

    Topics: Animals; Apoptosis; Brain Injuries, Traumatic; Corpus Striatum; Disease Models, Animal; Extracellular Signal-Regulated MAP Kinases; Male; MAP Kinase Kinase 4; MAP Kinase Signaling System; Mice; Neural Pathways; Neurodegenerative Diseases; Neurons; Neuroprotective Agents; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Random Allocation; Resveratrol; Stilbenes; Substantia Nigra

2017
Resveratrol attenuates neuronal autophagy and inflammatory injury by inhibiting the TLR4/NF-κB signaling pathway in experimental traumatic brain injury.
    International journal of molecular medicine, 2016, Volume: 37, Issue:4

    Previous research has demonstrated that traumatic brain injury (TBI) activates autophagy and a neuroinflammatory cascade that contributes to substantial neuronal damage and behavioral impairment, and Toll-like receptor 4 (TLR4) is an important mediator of this cascade. In the present study, we investigated the hypothesis that resveratrol (RV), a natural polyphenolic compound with potent multifaceted properties, alleviates brain damage mediated by TLR4 following TBI. Adult male Sprague Dawley rats, subjected to controlled cortical impact (CCI) injury, were intraperitoneally injected with RV (100 mg/kg, daily for 3 days) after the onset of TBI. The results demonstrated that RV significantly reduced brain edema, motor deficit, neuronal loss and improved spatial cognitive function. Double immunolabeling demonstrated that RV decreased microtubule-associated protein 1 light chain 3 (LC3), TLR4‑positive cells co-labeled with the hippocampal neurons, and RV also significantly reduced the number of TLR4‑positive neuron‑specific nuclear protein (NeuN) cells following TBI. Western blot analysis revealed that RV significantly reduced the protein expression of the autophagy marker proteins, LC3II and Beclin1, in the hippocampus compared with that in the TBI group. Furthermore, the levels of TLR4 and its known downstream signaling molecules, nuclear factor-κB (NF-κB), and the inflammatory cytokines, interleukin (IL)-1β and tumor necrosis factor (TNF)-α were also decreased after RV treatment. Our results suggest that RV reduces neuronal autophagy and inflammatory reactions in a rat model of TBI. Thus, we suggest that the neuroprotective effect of RV is associated with the TLR4/NF-κB signaling pathway.

    Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Autophagy; Brain; Brain Injuries, Traumatic; Male; Memory; Motor Activity; Neurons; Neuroprotective Agents; NF-kappa B; Rats, Sprague-Dawley; Resveratrol; Stilbenes; Toll-Like Receptor 4

2016
Neuroprotective effects of resveratrol against traumatic brain injury in rats: Involvement of synaptic proteins and neuronal autophagy.
    Molecular medicine reports, 2016, Volume: 13, Issue:6

    Traumatic brain injury (TBI) involves primary and secondary injury cascades that underlie delayed neuronal dysfunction and death, leading to long‑term cognitive deficits, and effective therapeutic strategies targeting neuronal death remain elusive. The present study aimed to determine whether the administration of resveratrol (100 mg/kg) was able to significantly enhance functional recovery in a rat model of TBI and whether resveratrol treatment was able to upregulate synaptic protein expression and suppress post‑TBI neuronal autophagy. The results demonstrated that daily treatment with resveratrol attenuated TBI‑induced brain edema and improved spatial cognitive function and neurological impairment in rats. The expression of synaptic proteins was downregulated following TBI and this phenomenon was partly reversed by treatment with resveratrol. In addition, resveratrol was observed to significantly reduce the levels of the autophagic marker proteins, microtubule‑associated protein light chain 3‑II and Beclin1, in the hippocampus compared with the TBI group. Therefore, these results suggest that resveratrol may represent a novel therapeutic strategy for TBI, and that this protection may be associated with the upregulation of synaptophysin, postsynaptic density protein 95 and the suppression of neuronal autophagy.

    Topics: Animals; Autophagy; Brain Injuries, Traumatic; Male; Neurons; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Resveratrol; Stilbenes; Synapses

2016
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