Background : Cerebral ischemia depletes ATP and causes irreversible tissue injury. Nicotinamide
is a precursor of NAD+ and it is also a poly (ADP-ribose) polymerase (PARP) inhibitor
that increases the neuronal ATP concentration and so protects against stroke. Therefore we
examined whether nicotinamide could protect against cerebral ischemia by using a model of
transient middle cerebral artery occlusion (MCAO) (reperfusion 2 h post ischemia) in Sprague-
Dawley rats. Methods : Nicotinamide (500 mg/kg) or normal saline was administered intraperitoneally
24 and 0 h before and after MCAO, respectively. The infarction volumes were determined
with triphenyltetrazolium chloride staining 24 h after reperfusion. The nitrotyrosine, PAR
polymer and PARP-1 expressions were examined by immunohistochemistry with using brain
slices obtained from the rats that were sacrificed at 0, 15, 30, 60 and 120 min after reperfusion.
expressions were increased at 0, 15 and 30 min, and those expressions for PARP polymer
and PARP-1 were increased at 60 and 120 min, respectively. Nicotinamide partly reduced
the expressions for nitrotyrosine and PAR polymer except for PARP-1. Conclusions : These
results suggest that nicotinamide may attenuate ischemic brain injury through its antioxidant
activity and the inhibition of PARP-1.