Cell and tissue damage in relation to apoptosis-linked molecules in experimental cerebral ischemia–reperfusion and traumatic spinal cord injury

Abstract

A variety of acute insults to the CNS, either traumatic, ischemic or inflammatory, bring about the destruction of neural tissue, leaving permanent damage. The mode of cell loss and tissue damage in those settings is thought to be either necrotic or apoptotic. However, the terms, necrosis and apoptosis, appear not well defined in solid tissues like brain, as opposed to freely circulating cells. We have attempted to assess the significance of death-related molecules and apoptosis for ultimately forming a mass of dead neural tissue, utilizing two experimental models of the CNS insult, i.e., acute transection injury of the spinal cord and ischemia–reperfusion damage of the cerebral hemisphere. Apoptosis-related molecules utilized here included p53, p21, Bcl-2, Bax for spinal cord injury model and p53 and NF-κB for ischemia–reperfusion.