Hydrogen-rich saline protects against oxidative damage and cognitive deficits after mild traumatic brain injury

@article{Hou2012HydrogenrichSP,
  title={Hydrogen-rich saline protects against oxidative damage and cognitive deficits after mild traumatic brain injury},
  author={Zong-gang Hou and Wei Luo and Xuejun Sun and Shuyu Hao and Ying Zhang and Feifan Xu and Zhong-cheng Wang and Baiyun Liu},
  journal={Brain Research Bulletin},
  year={2012},
  volume={88},
  pages={560-565}
}
Oxidative stress is the principal factor in traumatic brain injury (TBI) that initiates events that result in protracted neuronal dysfunction and remodeling. Importantly, antioxidants can protect the brain against oxidative damage and modulate the capacity of the brain to cope with synaptic dysfunction and cognitive impairment. However, no studies have investigated the effects of hydrogen-rich saline on cognitive deficits after TBI. In the present study, rats with fluid percussion injury (FPI… 
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References

SHOWING 1-10 OF 40 REFERENCES
Vitamin E Protects Against Oxidative Damage and Learning Disability After Mild Traumatic Brain Injury in Rats
TLDR
The results suggest that vitamin E dietary supplementation can protect the brain against the effects of mild TBI on synaptic plasticity and cognition, using molecular systems associated with the maintenance of long-term plasticity, such as BDNF and Sir2.
Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury.
TLDR
Early onset of oxidative stress suggests that the initial therapeutic window following TBI appears to be relatively short, and it may be necessary to stagger selective types of antioxidant therapy to target specific oxidative components.
Effect of melatonin on brain oxidative damage induced by traumatic brain injury in immature rats.
TLDR
Melatonin administered as a single dose of 5 mg/kg prevented the increase in TBARS levels in both non-traumatized and traumatized brain hemispheres, suggesting that melatonin protects against oxidative damage induced by TBI in the immature brain.
Antioxidant therapies in traumatic brain and spinal cord injury.
TLDR
The preclinical and clinical literature supporting the role of ROS and RNS and their derived oxygen free radicals in the secondary injury response following acute traumatic brain injury (TBI) and spinal cord injury (SCI) is covered and the past and current trends in the development of antioxidant therapeutic strategies are reviewed.
Oxidative stress in head trauma in aging.
TLDR
Overall, the data show increased levels of oxidative damage, diminished antioxidant capacities, and increased tissue loss in TBI in aging.
Peroxynitrite-mediated protein nitration and lipid peroxidation in a mouse model of traumatic brain injury.
TLDR
Investigation of the role of the ROS, peroxynitrite (PON), in the acute pathophysiology of TBI and its temporal relationship to neurodegeneration in the context of the mouse model of diffuse head injury model indicates that optimal pharmacological inhibition of post-traumatic oxidative damage in TBI may need to combine two functionalities.
Dietary curcumin supplementation counteracts reduction in levels of molecules involved in energy homeostasis after brain trauma
TLDR
Results show the potential of curcumin to regulate molecules involved in energy homeostasis following TBI, and may foster a new line of therapeutic treatments for TBI patients by endogenous upregulation of molecules important for functional recovery.
Hydrogen-rich saline improves memory function in a rat model of amyloid-beta-induced Alzheimer's disease by reduction of oxidative stress
TLDR
Hydrogen-rich saline prevented Abeta-induced neuroinflammation and oxidative stress, which may contribute to the improvement of memory dysfunction in this rat model.
Validation of brain extracellular glycerol as an indicator of cellular membrane damage due to free radical activity after traumatic brain injury.
TLDR
The data suggest that injury-induced increases in microdialysate glycerol levels are a valid indicator of free radical activity, and their amelioration following Tempol treatment accords with less histological damage in response to FPI.
Hydrogen-Rich Saline is Cerebroprotective in a Rat Model of Deep Hypothermic Circulatory Arrest
TLDR
HRS administration significantly attenuated the severity of DHCA induced brain injury by mechanisms involving amelioration of oxidative stress, down-regulation of inflammatory factors and reduction of apoptosis.
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