Proteomic Analysis of Cerebral Cortex Extracts from Sus scrofa with Induced Hemorrhagic Stroke

Cerebrovascular diseases, including stroke and micro stroke, are the main causes of death in contemporary society. Hemorrhagic stroke is the fast emerging defficiency in the brain function resulting from disturbance of blood supply to the brain caused by the rapture of blood vessels (Lopez et al. in Proteomics Clin Appl 6:190-200, 2012). The influence of a model hemorrhagic stroke on white pigs with the change in the protein profile of their cortical samples 24 h and 2 months after the stroke was examined using mass-spectrometric analysis. Different proteins (n = 30) were identified, and their content was elevated. These proteins are involved in the mechanisms of neuroprotection, including compensation of oxidative stress (TXN, SNCA, PRDX6, ENO1), prevention of unwanted protein aggregation and apoptosis (PTMA, SNCA, SNCB), release of neurotransmitters (GAPDH, PEBP1) and assembly of the cytoskeleton (ACTA2, PTMA, TUBA4A, TUBA1D), etc. Also, a group of seven Ras family proteins involved in the regulation of cell proliferation and differentiation was found in the samples taken 24 h following the stroke. The relative concentrations of most of the proteins in the samples taken 2 months after the stroke demonstrate intermediate values between the control sample and the sample taken in 24 h, indicating the extinction of change in the protein profile with time. During the first 24 h after the stroke, there is an increase in protein fractions participating in exocytosis, synaptic plasticity/signaling, and support of neurotransmitter transport. Such shift in the weight of protein functional clusters can be attributed to activation of compensatory mechanisms in the body focused on neuroprotection.