scholarly journals Gastrodin provides neuroprotection in models of traumatic brain injury via Nrf2 signaling pathway

2021 ◽  
Vol 13 (4) ◽  
pp. 62-69
Author(s):  
Dan Wang ◽  
Xiaoqing Dong
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuroprotective Effect ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Active Components ◽  
Nrf2 Pathway ◽  
Therapeutic Value ◽  
Nrf2 Signaling Pathway ◽  
Brain Tissues

Gastrodin is one of the main active components of Gastrodia elata and has significant therapeutic value for various nervous system diseases. Its medicinal properties include smooth muscle relaxation, anti-necrosis, anti-aging, and anti-apoptosis effects. However, its possible effects on traumatic brain injury (TBI) are still unclear. In this study, the effects of gastroditin on TBI rats were investigated. The results proved that gastrodin had neuroprotective effect on TBI through alleviating brain deficits, decreasing brain water content, inhibiting neuronal apoptosis, and suppressing oxidative stress in brain tissues of TBI rats. Mechanically, gastrodin upregulated the expression of Nrf2 downstream proteins, suggesting the activation of Nrf2 pathway in brain tissues of TBI rats. In conclusion, gastrodin provided neuroprotection in TBI rats via Nrf2 pathway.

Breviscapine provides a neuroprotective effect after traumatic brain injury by modulating the Nrf2 signaling pathway

2019 ◽  
Vol 120 (9) ◽  
pp. 14899-14907 ◽  
Author(s):  
Fayin Li ◽  
Xiaodong Wang ◽  
Zhijie Zhang ◽  
Pengfei Gao ◽  
Xianlong Zhang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Signaling Pathway ◽  
Neuroprotective Effect ◽  
Nrf2 Signaling Pathway

Pharmacological Benefits of Active Components of Natural Products Against Traumatic Brain Injury - A Review

2016 ◽  
Vol 13 (2) ◽  
pp. 99-116
Author(s):  
Selvaraju Subash ◽  
Musthafa M. Essa ◽  
Samir Al-Adawi ◽  
Mushtaq A. Memon ◽  
Thamilarasan Manivasagam ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Natural Products ◽  
Brain Injury ◽  
Active Components

The Neuroprotective Effect of Salubrinal in a Mouse Model of Traumatic Brain Injury

2015 ◽  
Vol 17 (1) ◽  
pp. 58-70 ◽  
Author(s):  
Vardit Rubovitch ◽  
Shani Barak ◽  
Lital Rachmany ◽  
Renana Baratz Goldstein ◽  
Yael Zilberstein ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mouse Model ◽  
Neuroprotective Effect

scholarly journals Regulatory T cells exhibit neuroprotective effect in a mouse model of traumatic brain injury

2016 ◽  
Vol 14 (6) ◽  
pp. 5556-5566 ◽  
Author(s):  
Yunhu Yu ◽  
Fang Cao ◽  
Qishan Ran ◽  
Xiaochuan Sun
Keyword(s):  
Traumatic Brain Injury ◽  
T Cells ◽  
Brain Injury ◽  
Regulatory T Cells ◽  
Mouse Model ◽  
Neuroprotective Effect

scholarly journals Traumatic Brain Injury: Oxidative Stress and Novel Anti-Oxidants Such as Mitoquinone and Edaravone

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 943 ◽  
Author(s):  
Helene Ismail ◽  
Zaynab Shakkour ◽  
Maha Tabet ◽  
Samar Abdelhady ◽  
Abir Kobaisi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuroprotective Effect ◽  
Treatment Options ◽  
Free Radical Scavenger ◽  
Health Concern ◽  
Radical Scavenger ◽  
History Of ◽  
Ionic Imbalance

Traumatic brain injury (TBI) is a major health concern worldwide and is classified based on severity into mild, moderate, and severe. The mechanical injury in TBI leads to a metabolic and ionic imbalance, which eventually leads to excessive production of reactive oxygen species (ROS) and a state of oxidative stress. To date, no drug has been approved by the food and drug administration (FDA) for the treatment of TBI. Nevertheless, it is thought that targeting the pathology mechanisms would alleviate the consequences of TBI. For that purpose, antioxidants have been considered as treatment options in TBI and were shown to have a neuroprotective effect. In this review, we will discuss oxidative stress in TBI, the history of antioxidant utilization in the treatment of TBI, and we will focus on two novel antioxidants, mitoquinone (MitoQ) and edaravone. MitoQ can cross the blood brain barrier and cellular membranes to accumulate in the mitochondria and is thought to activate the Nrf2/ARE pathway leading to an increase in the expression of antioxidant enzymes. Edaravone is a free radical scavenger that leads to the mitigation of damage resulting from oxidative stress with a possible association to the activation of the Nrf2/ARE pathway as well.

scholarly journals Xenon treatment after severe traumatic brain injury improves locomotor outcome, reduces acute neuronal loss and enhances early beneficial neuroinflammation: a randomized, blinded, controlled animal study

Critical Care ◽  
2020 ◽  
Vol 24 (1) ◽  
Author(s):  
Rita Campos-Pires ◽  
Haldis Onggradito ◽  
Eszter Ujvari ◽  
Shughoofa Karimi ◽  
Flavia Valeo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcome ◽  
Neuroprotective Effect ◽  
Neuronal Loss ◽  
Brain Trauma ◽  
Lesion Volume ◽  
Oxygen Balance ◽  
Sprague Dawley ◽  
Locomotor Deficits

Abstract Background Traumatic brain injury (TBI) is a major cause of morbidity and mortality, but there are no clinically proven treatments that specifically target neuronal loss and secondary injury development following TBI. In this study, we evaluate the effect of xenon treatment on functional outcome, lesion volume, neuronal loss and neuroinflammation after severe TBI in rats. Methods Young adult male Sprague Dawley rats were subjected to controlled cortical impact (CCI) brain trauma or sham surgery followed by treatment with either 50% xenon:25% oxygen balance nitrogen, or control gas 75% nitrogen:25% oxygen. Locomotor function was assessed using Catwalk-XT automated gait analysis at baseline and 24 h after injury. Histological outcomes were assessed following perfusion fixation at 15 min or 24 h after injury or sham procedure. Results Xenon treatment reduced lesion volume, reduced early locomotor deficits, and attenuated neuronal loss in clinically relevant cortical and subcortical areas. Xenon treatment resulted in significant increases in Iba1-positive microglia and GFAP-positive reactive astrocytes that was associated with neuronal preservation. Conclusions Our findings demonstrate that xenon improves functional outcome and reduces neuronal loss after brain trauma in rats. Neuronal preservation was associated with a xenon-induced enhancement of microglial cell numbers and astrocyte activation, consistent with a role for early beneficial neuroinflammation in xenon’s neuroprotective effect. These findings suggest that xenon may be a first-line clinical treatment for brain trauma.

scholarly journals Reduction of Traumatic Brain Damage by Tspo Ligand Etifoxine

2019 ◽  
Vol 20 (11) ◽  
pp. 2639 ◽  
Author(s):  
Mona Shehadeh ◽  
Eilam Palzur ◽  
Liat Apel ◽  
Jean Francois Soustiel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Potential Effect ◽  
Translocator Protein ◽  
Male Rats ◽  
Lesion Volume ◽  
Sprague Dawley

Experimental studies have shown that ligands of the 18 kDa translocator protein can reduce neuronal damage induced by traumatic brain injury by protecting mitochondria and preventing metabolic crisis. Etifoxine, an anxiolytic drug and 18 kDa translocator protein ligand, has shown beneficial effects in the models of peripheral nerve neuropathy. The present study investigates the potential effect of etifoxine as a neuroprotective agent in traumatic brain injury (TBI). For this purpose, the effect of etifoxine on lesion volume and modified neurological severity score at 4 weeks was tested in Sprague–Dawley adult male rats submitted to cortical impact contusion. Effects of etifoxine treatment on neuronal survival and apoptosis were also assessed by immune stains in the perilesional area. Etifoxine induced a significant reduction in the lesion volume compared to nontreated animals in a dose-dependent fashion with a similar effect on neurological outcome at four weeks that correlated with enhanced neuron survival and reduced apoptotic activity. These results are consistent with the neuroprotective effect of etifoxine in TBI that may justify further translational research.

scholarly journals Docosahexaenoic Acid Protects Traumatic Brain Injury by Regulating NOX2 Generation via Nrf2 Signaling Pathway

2020 ◽  
Vol 45 (8) ◽  
pp. 1839-1850
Author(s):  
Wei Zhu ◽  
Guangqiang Cui ◽  
Tuo Li ◽  
Hongguang Chen ◽  
Jian Zhu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Docosahexaenoic Acid ◽  
Signaling Pathway ◽  
Nrf2 Signaling Pathway
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