JNK/p38 MAPK involves in ginsenoside Rb1 attenuating beta-amyloid peptide (25-35) -induced tau protein hyperphosphorylation in embryo rat cortical neurons
Song, J-Qiu.; Chen, X-Chun.; Zhang, J.; Huang, T-Wen.; Zeng, Y-Qi.; Shen, J.; Chen, L-Min.
Yao Xue Xue Bao 43(1): 29-34
2008
ISSN/ISBN: 0513-4870 PMID: 18357728 Document Number: 616461
To explore the effect of ginsenoside Rb1 on JNK/p38 MAPK in the process of beta-amyloid peptide (25-35)-induced tau protein hyperphosphorylation, Western blotting and immunocytochemical stain were performed to observe the tau protein phosphorylation and the expression of JNK/p38 MAPK. The level of tau protein phosphorylation in the sites of Ser(396), Ser(199/202) and Thr(205) increased after rat cortical neurons exposed to 20 mu mol.L-1 A beta(25-35), meanwhile the level of JNK/p38 MAPK also increased after A beta(25-35) treatment for 12 h. Pretreatment with several doses of ginsenoside Rb1 markedly attenuated tau protein hyperphosphorylation and the expression of JNK/p38 MAPK. Ginsenoside Rb1 markedly attenuated tau protein hyperphosphorylation through JNK/p38 MAPK pathway.