Effects of selective and non-selective cyclooxygenase inhibition against neurological deficit and brain oedema following closed head injury in mice.

The implication of cyclooxygenase (COX) type 2 in post-traumatic consequences is so far controversial. In experimental models of traumatic brain injury (TBI), genetic disruption or pharmacological inhibition of COX-2 has been shown to be neuroprotective, deleterious or without effect. Therefore, the aim of our study was to investigate the effect of COX-2 inhibition against neurological deficit and brain oedema after TBI that was induced by mechanical percussion in male Swiss mice.

Neuroblast survival depends on mature vascular network formation after mouse stroke: role of endothelial and smooth muscle progenitor cell co-administration.

Pro-angiogenic cell-based therapies constitute an interesting and attractive approach to enhancing post-stroke neurogenesis and decreasing neurological deficit. However, most new stroke-induced neurons die during the first few weeks after ischemia, thus impairing total recovery. Although the neovascularization process involves different cell types and various growth factors, most cell therapy protocols are based on the biological effects of single-cell-type populations or on the administration of heterogeneous populations of progenitors, namely human cord blood-derived CD34(+) cells, with scarce vascular progenitor cells.

Simvastatin in traumatic brain injury: effect on brain edema mechanisms.

Objectives: Traumatic brain injury causes deleterious brain edema, leading to high mortality and morbidity. Brain edema exacerbates neurologic deficits and may be attributable to the breakdown of endothelial cell junction protein, leukocyte infiltration, and matrix metalloproteinase activation. These all contribute to loss of blood-brain barrier integrity.