Topic: oxidative damage

Traumatic brain injury (TBI) can cause life-changing neurological deficits. There are currently no neuroprotective treatments in TBI. The high content of oxidation-sensitive polyunsaturated fatty acids (PUFAs) in the brain generates an environment vulnerable to TBI-related oxidative damage. We hypothesised that partial replacement of tissue PUFAs with deuterium - enriched PUFAs (D-PUFAs), could act as a brake against oxidation and improve outcome.A moderately severe TBI was induced using a controlled cortical impact (CCI) in adult male and female CD1 mice. Animals received a control or a D-PUF

In the present study, we validated the neuroprotective effects of sulfiredoxin 1 (SRXN1) protein against oxidative damage in HT22 cells and ischemic damage in gerbil hippocampus. To deliver SRXN1 protein into cells or hippocampus, PEP-1-SRXN1 fusion protein was synthesized and the efficient delivery was visualized in HT22 cells and gerbil hippocampus. In addition, the treatment of PEP-1-SRXN1 was delivered in HT22 cells with concentration- and incubation time-dependent manners. In addition, PEP-1-SRXN1 treatment significantly ameliorated formation of reactive oxygen species and cell death in H