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<0.05), and the infarct volume was decreased in Low dose group (P<0.05). Consistent with these results, immunohistochemistry and Western blot analysis indicated that TRAF6 expression was significantly decreased in SOP administrated groups at 24 h, and the expression of phosphorylated ERK1/2 increased in Low dose at 72 h. 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.
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<0.05), and the infarct volume was decreased in Low dose group (P<0.05). Consistent with these results, immunohistochemistry and Western blot analysis indicated that TRAF6 expression was significantly decreased in SOP administrated groups at 24 h, and the expression of phosphorylated ERK1/2 increased in Low dose at 72 h. 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.