Inflammation and oxidative stress play an important role in cerebral ischemic pathogenesis.
Polydatin has been proved to elicit numerous
biological effects through its anti-inflammatory and
anti-oxidant properties. However, little is known regard to the mechanism of
polydatin's neuroprotection in
ischemic stroke. We therefore investigated the potential
neuroprotective effects of
polydatin and explored the underlying mechanisms. Male, Sprague-Dawley rats were subjected to permanent
middle cerebral artery occlusion (pMCAO). Experiment 1 was used to evaluate the expression of
glioma-associated oncogene homolog1 (Gli1), Patched-1 (Ptch1) and
Superoxide dismutase 1 (SOD1) after pMCAO, six time points were included. Experiment 2 was used to detect
polydatin's neuroprotection after pMCAO. Neurological deficit, brain water content and
infarct size were measured at 24h and 72 h after pMCAO. Immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR), Western Blotting, activity assay and confocal microscope were used to analyse the expression of Gli1, Ptch1, SOD1 and
nuclear factor-kappa B (NF-κB). Experiment 3 was used to detect
polydatin's influence on blood-brain barrier (BBB). Compared with
Sham group, the expression of Gli1, Ptch1 and SOD1 were up-regulated shortly after pMCAO (P<0.05). Compared with Vehicle group, high dose of
polydatin (50mg/kg) up-regulated Gli1, Ptch1, SOD1 and down-regulated NF-κB, and reduced
infarct volume, brain water content and behavioral deficits (P<0.05). Meanwhile, BBB permeability was also ameliorated. The results indicated that
polydatin protected the brain from damage caused by pMCAO, and this effect may be through up-regulating the expression of Gli1, Ptch1 and SOD1 and down-regulating the expression of NF-κB, and ameliorating BBB permeability.