Neuroprotective Effects of XXXX Against Focal @entity2806 /Reperfusion Injury in @entity35 Through Attenuation of Inflammation.

@entity5045 @entity32 @entity64 @entity2806 @entity63 @entity2500 @entity12149 @entity16 @entity568 @entity1505 @entity3089 @entity3090 @entity1188 @entity842 @entity3426 @entity35 @entity204
@entity64 is the second leading cause of @entity204 among adults worldwide. @entity3089 ( @entity3090 ) has been demonstrated to exhibit neuroprotective functions in @entity2806 /reperfusion injury. However, the underlying mechanisms in this process and its contribution to the protection function remain unknown. The current study examined the neuroprotective effects of @entity3090 after transient @entity2500 (tMCAO) in @entity35 . tMCAO for 120 min was induced in male @entity35 treated with @entity3090 (50 mg/kg, i.p.) or Vehicle immediately after reperfusion. Neurological score, @entity1188 ratio and inflammation-related molecules (assessed by @entity5045 , enzyme-linked immunosorbent assays, quantitative real-time PCR or western blotting) were estimated at 24 h after operation. @entity3090 prevented the @entity16 and decreased the @entity1188 volume, compared with the Vehicle group. The inflammation-related molecules @entity1505 , @entity3426 , @entity568 levels usually caused by @entity63 /reperfusion were significantly ameliorated by @entity3090 . @entity3090 also inhibited the upregulation of nuclear factor-kappa B/ @entity12149 (NF-kB/ @entity12149 ), and induction of cyclooxygenase 2 and inducible @entity842 synthase. The present study indicates that @entity3090 may be a promising therapeutic agent for @entity2806 /reperfusion injury through @entity32 .
