Glial fibrillary acidic protein levels are associated with global histone H4 acetylation after spinal cord injury in rats

Emerging evidence has suggested global histone H4 acetylation status plays an important role in neural plasticity. For instance, the imbalance of this epigenetic marker has been hypothesized as a key factor for the development and progression of several neurological diseases. Likewise, astrocytic reactivity-a wellknown process that markedly influences the tissue remodeling after a central nervous system injury-is crucial for tissue remodeling after spinal cord injury（SCI）. However, the linkage between the above-mentioned mechanisms after SCI remains poorly understood. We sought to investigate the relation between both glial fibrillary acidic protein（GFAP） and S100 calcium-binding protein B（S100B）（astrocytic reactivity classical markers） and global histone H4 acetylation levels. Sixty-one male Wistar rats（aged ~3 months） were divided into the following groups： sham; 6 hours post-SCI; 24 hours post-SCI; 48 hours post-SCI; 72 hours post-SCI; and 7 days post-SCI. The results suggested that GFAP, but not S100B was associated with global histone H4 acetylation levels. Moreover, global histone H4 acetylation levels exhibited a complex pattern after SCI, encompassing at least three clearly defined phases（first phase： no changes in the 6, 24 and 48 hours post-SCI groups; second phase： increased levels in the 72 hours post-SCI group; and a third phase： return to levels similar to control in the 7 days post-SCI group）. Overall, these findings suggest global H4 acetylation levels exhibit distinct patterns of expression during the first week post-SCI, which may be associated with GFAP levels in the perilesional tissue. Current data encourage studies using H4 acetylation as a possible biomarker for tissue remodeling after spinal cord injury.

Association of Serum Antioxidant Enzymes and Nervous Tissue Markers in Hypertensive Patients

Background and Purpose: Hypertension has serious effects on cerebral blood vessels. Oxidative stress seems to be implicated in blood pressure elevation, through increased reactive oxygen species and/or decreased antioxidant capacity. Recently blood markers indicating damage to the central nervous system were reported to be increased in hypertensive patients. However, it is unknown whether antioxidant capacity is related to these changes. This study was designed to explore if the concentration of blood markers for nervous tissue damage was associated to antioxidant capacity in hypertensive patients. Methods: Twenty hypertensive patients and 23 healthy controls were studied. They were paired by age, sex, ethnicity, or risk factors. Serum neuron specific enolase (NSE) and S100 calcium binding protein B (S100B) were measured as nervous tissue damage markers, as well as the activity of antioxidant enzymes (catalase, glutathione peroxidase, glutathione reductase and gamma-glutamyltransferase). Results: Serum neuronal specific enolase (NSE) and S100 calcium binding protein B (S100B) concentrations determined by immunoassay were significantly increased in patients vs. controls. The activities of antioxidant enzymes measured by spectrophotometry showed that plasmatic catalase and erythrocytic glutathione peroxidase were significantly increased in patients, but erythocytic catalase was decreased. Gamma-glutamyltransferase activity was significantly correlated with S100B in hypertensive patients, while erythrocytic catalase activity was decreased in subjects with higher NSE levels. Conclusion: This preliminary investigation suggested that antioxidant status might be modulated through changes in antioxidant enzymatic activity in hypertensive patients. The association of some of these changes with peripheral markers of damage to the central nervous system could indicate that the increased levels of these proteins in hypertension are partly related to oxidative stress.