The objective of this study was to evaluate whether
Tanshinone IIA (
TSA) was neuroprotective in permanent focal
cerebral ischemia and to determine the possible mechanisms of its neuroprotection. Mice were subjected to permanent
middle cerebral artery occlusion. The neuroprotection of
TSA was investigated with respect to neurological deficit scores and
infarct volume. Biochemical analyses for
malondialdehyde (MDA) content and
superoxide dismutase (SOD) activity in serum, and
nitric oxide (NO) content and the
inducible nitric oxide synthase (iNOS) activity in brain tissue were performed at 24 h after
ischemia. Immunohistochemistry was used to measure the expression of iNOS. In vitro, the effects of
TSA were tested in the cultured astrocytes exposed to
hydrogen dioxide (H2O2).
TSA (5, 10 and 20 mg/kg, i.p.) significantly reduced the
infarct volume and improve neurological deficit.
TSA also significantly increased the activity of SOD after 24 h of
ischemia and decreased the MDA level, NO content, and iNOS expression. In vitro, the translocation of
NF-kappaB was inhibited by
TSA and the survival rate of astrocytes was markedly increased and the NO production was decreased. In conclusion, these results illustrated that
TSA protected the brain from ischemic injury by suppressing the oxidative stress and the radical-mediated inflammatory insult.