scholarly journals Astaxanthin Activates Nuclear Factor Erythroid-Related Factor 2 and the Antioxidant Responsive Element (Nrf2-ARE) Pathway in the Brain after Subarachnoid Hemorrhage in Rats and Attenuates Early Brain Injury

Marine Drugs ◽  
2014 ◽  
Vol 12 (12) ◽  
pp. 6125-6141 ◽  
Author(s):  
Qi Wu ◽  
Xiang-Sheng Zhang ◽  
Han-Dong Wang ◽  
Xin Zhang ◽  
Qing Yu ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Early Brain Injury ◽  
Related Factor ◽  
Nuclear Factor ◽  
Responsive Element ◽  
The Brain ◽  
Antioxidant Responsive Element

scholarly journals Nuclear Factor-E2-related Factor-1 Mediates Ascorbic Acid Induction of Osterix Expression via Interaction with Antioxidant-Responsive Element in Bone Cells

2007 ◽  
Vol 282 (30) ◽  
pp. 22052-22061 ◽  
Author(s):  
Weirong Xing ◽  
Anny Singgih ◽  
Anil Kapoor ◽  
Catrina M. Alarcon ◽  
David J. Baylink ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Bone Cells ◽  
Related Factor ◽  
Nuclear Factor ◽  
Responsive Element ◽  
Antioxidant Responsive Element

scholarly journals Clinical Trials in Cardiac Arrest and Subarachnoid Hemorrhage: Lessons from the Past and Ideas for the Future

2013 ◽  
Vol 2013 ◽  
pp. 1-42
Author(s):  
Jennifer A. Frontera
Keyword(s):  
Clinical Trials ◽  
Cardiac Arrest ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Randomized Clinical Trials ◽  
Early Brain Injury ◽  
Aneurysm Rupture ◽  
Neurological Outcomes ◽  
Injury Research ◽  
The Brain

Introduction. Elevated intracranial pressure that occurs at the time of cerebral aneurysm rupture can lead to inadequate cerebral blood flow, which may mimic the brain injury cascade that occurs after cardiac arrest. Insights from clinical trials in cardiac arrest may provide direction for future early brain injury research after subarachnoid hemorrhage (SAH).Methods. A search of PubMed from 1980 to 2012 and clinicaltrials.gov was conducted to identify published and ongoing randomized clinical trials in aneurysmal SAH and cardiac arrest patients. Only English, adult, human studies with primary or secondary mortality or neurological outcomes were included.Results. A total of 142 trials (82 SAH, 60 cardiac arrest) met the review criteria (103 published, 39 ongoing). The majority of both published and ongoing SAH trials focus on delayed secondary insults after SAH (70%), while 100% of cardiac arrest trials tested interventions within the first few hours of ictus. No SAH trials addressing treatment of early brain injury were identified. Twenty-nine percent of SAH and 13% of cardiac arrest trials showed outcome benefit, though there is no overlap mechanistically.Conclusions. Clinical trials in SAH assessing acute brain injury are warranted and successful interventions identified by the cardiac arrest literature may be reasonable targets of the study.

Dimethylfumarate alleviates early brain injury and secondary cognitive deficits after experimental subarachnoid hemorrhage via activation of Keap1-Nrf2-ARE system

2015 ◽  
Vol 123 (4) ◽  
pp. 915-923 ◽  
Author(s):  
Yizhi Liu ◽  
Jiaoxue Qiu ◽  
Zhong Wang ◽  
Wanchun You ◽  
Lingyun Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Neuroprotective Effect ◽  
Autologous Blood ◽  
Early Brain Injury ◽  
Related Factor ◽  
Learning Deficits

OBJECT Oxidative stress and the inflammatory response are thought to promote brain damage in the setting of subarachnoid hemorrhage (SAH). Previous reports have shown that dimethylfumarate (DMF) can activate the Kelch-like ECH-associated protein 1–nuclear factor erythroid 2-related factor 2–antioxidant-responsive element (Keap1-Nrf2-ARE) system in vivo and in vitro, which leads to the downregulation of oxidative stress and inflammation. The aim of this study was to evaluate the potential neuroprotective effect of DMF on SAH-induced brain injury in rats. METHODS Rats were subjected to SAH by the injection of 300 μl of autologous blood into the chiasmatic cistern. Rats in a DMF-treated group were given 15 mg/kg DMF twice daily by oral gavage for 2 days after the onset of SAH. Cortical apoptosis, neural necrosis, brain edema, blood-brain barrier impairment, learning deficits, and changes in the Keap1-Nrf2-ARE pathway were assessed. RESULTS Administration of DMF significantly ameliorated the early brain injury and learning deficits induced by SAH in this animal model. Treatment with DMF markedly upregulated the expressions of agents related to Keap1-Nrf2-ARE signaling after SAH. The inflammatory response and oxidative stress were downregulated by DMF therapy. CONCLUSIONS DMF administration resulted in abatement of the development of early brain injury and cognitive dysfunction in this prechiasmatic cistern SAH model. This result was probably mediated by the effect of DMF on the Keap1-Nrf2-ARE system.

scholarly journals Curcumin Plays Neuroprotection Activity by Modulation of Neurotrophic Factor BDNF, GAP-43 and GFAP in Mice with Traumatic Brain Injury (P06-043-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Nurhan Sahin ◽  
Ertugrul Kilic ◽  
Nilay Ates ◽  
Zeynep Balcikanli ◽  
Cemal Orhan ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurotrophic Factor ◽  
Infarct Volume ◽  
Intraperitoneal Administration ◽  
Vehicle Group ◽  
Related Factor ◽  
Nuclear Factor ◽  
Health Technologies ◽  
The Brain

Abstract Objectives Curcumin, extracted from the rhizome Curcuma longa, has been shown to be beneficial for neuroprotection in previous studies. In a recent study, a novel formulation of curcumin resulted in an increased relative absorption by 46 times (CurcuWIN®) of the total curcuminoids over the unformulated standard curcumin form. However, the exact mechanisms by which curcumin demonstrates its neuroprotective effects are not fully understood. The present study aimed to investigate the effects of curcumin supplementation on the expression of brain-derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), a main component of the glial scar, and growth-associated protein-43 (GAP-43), a signaling molecule in traumatic brain injury (TBI). Methods Brain injury was induced using a cold trauma model in male mice that were treated with curcumin (50 mg/kg) or vehicle via intraperitoneal administration just after TBI. Mice were divided into two groups: TBI + vehicle group and TBI + curcumin (CurcuWIN) group. Results The results show that curcumin treatment reduced the infarct volume in the brain. TBI induction increased inflammatory cytokines (IL-1β and IL-6), nuclear factor-κB (NF-κB) and GFAP, and reduced BDNF, GAP-43, neural cell adhesion molecule (ICAM) and nuclear factor erythroid 2-related factor 2 (Nrf2) levels in the brain. Interestingly, curcumin decreased the levels of NF-κB, IL-1β, IL-6, and GFAP, and increased BDNF, GAP-43, ICAM and Nrf2 levels in the brain. Conclusions In conclusion, these results showed that curcumin could increase the levels of BDNF, GAP-43, ICAM, and Nrf2 and attenuate brain injury in the model of TBI. Funding Sources This study was supported by OmniActive Health Technologies Inc. (NJ, USA). This work was also supported in part by the Turkish Academy of Sciences. Supporting Tables, Images and/or Graphs

Sign in / Sign up

Export Citation Format

Share Document