The Investigation Of Smad4 Expression In Hippocampus After Brain I/R Injury And NBP Treated Rats And Subcellular Compartmentalization Of Smad4 In Golgi Apparatus

Objective:To investigate the protective mechanisms of NBP after transient brain ischemia, and further study of expression changes and subcellular localization of smad4 in ratsMethods:(1) Animal Groups:Fifty healthy male SD rats, devided into four groups:Normal Group (n=5); Sham Operation Group (n=5); Ischemia Reperfusion Group (I/R) (n=20); NBP Intervention Group (NI/R) (n=20); I/R Group and NI/R Group are devided into four subgroups (each group n=5):6 hours,1 day,3 days,7 days after I/R ingury; (2) Models:15 minutes'common carotid artery occlusion(CAO) of both sides and reperfusion for 6 hours,1 day,3 days,7 days,Sodium Nitroprusside (SNP)control low blood pressure in Rats; The Sham Operation Group only give segregation but no occlusion; gavage of NBP(80mg/kg,BID) until death,;(3)HE Staining; (4)Immunohistochemistry.(5) Confocal Immuno-fluorographs of Smad4 and TGN46 were taken in rats models postocclusionResults:There were significant histological changes and elevated expression of Smad4 protein in I/R group compared with sham operation group in the hippocampus of the Rats,6h expression increased, 1d moderately increased,3d and 7d highest.P<0.05compared with the sham operation group; The histological changes in hippocampus of CA1 were significantly increased in NBP group compared with I/R group(P<0.05). Smad4 was colocalized with TGN46,a marker molecule for the Golgi apparatus.Conclusions:1. Expressions of Smad4 in hippocampus of CA3 of rats were significantly increased following cerebral ischemia-reperfusion, this suggested that the increased expressions of Smad4 could have protected the brain tissue from damage.2. NBP can relieve the brain damage induced by focal I/R in rats, which may be correlated with the inhibition of expression of Smad4.3. Smad4 was presented in the Golgi apparatus, suggesting that both continuous protein synthesis and transportation via the Golgi complex were required for Smad4 secretion and Smad4 may be essential for physiological functions involving GA...