Neuroprotective effect of early and short-time applying sophoridine in pMCAO rat brain: down-regulated TRAF6 and up-regulated p-ERK1/2 expression, ameliorated brain infaction and edema.

Abstract Background Matrine has been proven to protect ischemic injury in brain and sophoridine (SOP) is an isomeride of matrine. It is unknown whether SOP has this protective effect on ischemic injury in brain. We therefore investigated the potential neuroprotective role of SOP and the underlying mechanism. Methods Male, Sprague-Dawley rats were randomly assigned into five groups: Vehicle (pMCAO + saline), High dose (pMCAO + SOP 10 mg/kg), Middle dose (pMCAO + SOP 5 mg/kg), Low dose (pMCAO + SOP 2.5 mg/kg) and Sham operated group. Permanent middle cerebral artery occlusion (pMCAO) model was used and SOP was administered intraperitoneally immediately after cerebral ischemia and once daily in the following days. Neurological deficit was evaluated using a modified six point scale; brain water content and infarct volume were measured. The expression of TRAF6 and ERK1/2 were measured by immunohistochemistry, Western blotting. Results Compared with Vehicle group, the cerebral edema was alleviated in High dose group ( P P Conclusions SOP protected the brain from damage caused by pMCAO, and this effect may be through down-regulation of TRAF6 expression and up-regulation of ERK1/2 phosphorylation expression.