Oxymatrine protects rat brains against permanent focal ischemia and downregulates NF-κB expression

Background: Oxymatrine is proven to protect ischemic and reperfusion injury in liver, intestine and heart, this effect is via anti-inflammation and anti-apoptosis. Whether this protective effect applies to ischemic injury in brain, we therefore investigate the potential neuroprotective role of oxymatrine and the underlying mechanisms. Methods: Male, Sprague-Dawley rats were randomly assigned to four groups: permanent middle cerebral artery occlusion (pMCAO), high dose (pMCAO+oxymatrine 120 mg/kg), low dose (pMCAO+ oxymatrine 60 mg/kg) and sham operated group. We used a permanent middle cerebral artery occlusion model and administered oxymatrine intraperitoneally immediately after cerebral ischemia and once daily on the following days. At 24 h after MCAO, neurological deficit was evaluated using a modified six point scale; brain water content was measured; NF-kappa B expression was measured by immunohistochemistry, Western blotting and RT-PCR. Infarct volume was analyzed with 2, 3, S-triphenyltetrazolium chloride (TTC) staining at 72 h. Results: Compared with pMCAO group, neurological deficit in high dose group was improved (P<0.05), infarct volume was decreased (P<0.001) and cerebral edema was alleviated (P<0.05). Consistent with these indices, immunohistochemistry, Western blot and RT-PCR analysis indicated that NF-kappa B expression was significantly decreased in high dose group. Low dose of oxymatrine did not affect NF-kappa B expression in pMCAO rats. Conclusions: Oxymatrine reduced infarct volume induced by pMCAO, this effect may be through the decreasing of NF-kappa B expression. (C) 2009 Elsevier B.V. All rights reserved.