N-acetylcysteine (NAC): Brain First Aid
 N-acetylcysteine reduces lipopolysaccharide-sensitized hypoxic-ischemic brain injury
Wang, X., Svedin, P., Nie, C., Lapatto, R., Zhu, C., Gustavsson, M., . . . Mallard, C. (2007). N-acetylcysteine reduces lipopolysaccharide-sensitized hypoxic-ischemic brain injury. Annals of Neurology,61(3), 263-271. doi:10.1002/ana.21066
NAC (200mg/kg) provided marked neuroprotection with up to 78% reduction of brain injury in the pre+post-HI treatment group and 41% in the early (0 hour) post-HI treatment group, which was much more pronounced protection than another free radical scavenger, melatonin. Protection by NAC was associated with the following factors: (1) reduced isoprostane activation and nitrotyrosine formation; (2) increased levels of the antioxidants glutathione, thioredoxin-2, and (3) inhibition of caspase-3, calpain, and caspase-1 activation.
 Early, Transient Increase in Complexin I and Complexin II in the Cerebral Cortex following Traumatic Brain Injury Is Attenuated by N-Acetylcysteine
Yi, J., Hoover, R., Mcintosh, T. K., & Hazell, A. S. (2006). Early, Transient Increase in Complexin I and Complexin II in the Cerebral Cortex following Traumatic Brain Injury Is Attenuated by N-Acetylcysteine. Journal of Neurotrauma,23(1), 86-96. doi:10.1089/neu.2006.23.86
… The early, transient increase in the injured cortex was completely blocked by N-acetylcysteine (NAC) administered 5 min following trauma, suggesting an involvement of oxidative stress. Neuronal loss was also reduced in the injured hemisphere with post-TBI NAC treatment. Our findings suggest a dysregulation of both inhibitory and excitatory neurotransmission following traumatic injury that is responsive to antioxidant treatment. These alterations in complexin levels may also play an important role in neuronal cell loss following TBI, and thus contribute to the pathophysiology of cerebral damage following brain injury.
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