N-acetylcysteine amide confers neuroprotection, improves bioenergetics and behavioral outcome following TBI.

摘要: Traumatic brain injury (TBI) has become a growing epidemic but no approved pharmacological treatment been identified. Our previous work indicates that mitochondrial oxidative stress/damage and loss of bioenergetics play pivotal role in neuronal cell death behavioral outcome following experimental TBI. One tactic had some success is to target glutathione using its precursor N-acetylcysteine (NAC). However, this approach hindered by the low CNS bioavailability NAC. The current study evaluated novel, permeant amide form (NACA), which high permeability through cellular membranes resulting increased bioavailability. Cortical tissue sparing, cognitive function stress markers were assessed rats treated with NACA, NAC, or vehicle At 15days post-injury, animals NACA demonstrated significant improvements cortical sparing compared NAC animals. also was shown reduce damage (HNE levels) at 7days post-injury. Mechanistically, post-injury administration maintain levels comparable sham Collectively these data provide basic platform consider as novel therapeutic agent for