CONCLUSIONS : These inflammatory mediators may be predictive of a poor outcome in patients with traumatic brain injury in which contusions are the predominant abnormality.
Cerebral inflammation involves molecular cascades contributing to progressive damage after traumatic brain injury (TBI).
PARP contributes to neuronal cell death in vivo after cerebral ischemia/reperfusion , however , the role of PARP in the pathogenesis of traumatic brain injury (TBI) is unknown.
beta-Lapachone inhibited PARP , apparently by direct interaction with the enzyme.