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JNK/P38 MAPK Involved In Ginsenoside Rb1 And Rg1 Attenuating Beta-amyloid Peptide 25-35-induced Tau Protein Hyperphosphorylation In Embryo Rat Cortical Neurons

Posted on:2007-08-26Degree:MasterType:Thesis
Country:ChinaCandidate:J Q SongFull Text:PDF
GTID:2144360185485060Subject:Neurology
Abstract/Summary:PDF Full Text Request
Objective To investigate the effect and the molecular mechanism of aggregated beta-amyloid peptide 25-35 (Aβ25-35) on the level of tau protein phosphorylation in embryo rat cortical neurons through nNOS-JNK/p38MAPK ways, and to explore the protective effect of gisenoside Rb1 and gisenoside Rgl on Aβ25-35-induced tau protein hyperphosporylation and their mechamism of activation of JNK/p38MAPK.Method Primary cultures of cortical neurons were prepared from the embryonic day 18±2 Sprague-Dawley rats. And choose appropriate concentration of Aβ25-35. wesern-blot and immunocytochemical stain were performed to observe the tau protein phosphorylation and the expression of JNK/p38MAPK or nNOS when neurons exprosed to 20μmol/L Aβ25-35 in the prescene or...
Keywords/Search Tags:ginsenoside, β-amyloid peptide 25-35 (Aβ25-35), tau protein, phosphorylation, c-jun N-terminal kinase, p38MAPK, Neuronal nitric oxide kinases
PDF Full Text Request
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