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MCI186 to reduce A140 PC12 cells induced phosphorylation of tau
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MCI186 to reduce A140 PC12 cells induced phosphorylation of tau
[Abstract] Objective of edaravone (MCI 186) of the amyloid protein (A1 40) induced tau protein phosphorylation in PC12 cells and its mechanism of protection. Methods such as Western blot detection of Ser396, Ser199/202, Tau 5 and GSK 3, GSK 3Ser9 phosphorylation observed MCI 186 A25 35 induced injury in PC12 cells. The results of model group tau protein in Ser396, Ser199/202 phosphorylation sites and total tau protein levels in A1 40 role began to increase after 3 h, while the expression of GSK 3 increased the expression of phosphorylated GSK 3Ser9 reduction, MCI 186 protection group tau protein in the Ser396, Ser199/202 phosphorylation sites and total tau protein levels were significantly lower than A model group (P lt;0.05), GSK 3 expression is reduced, the expression of phosphorylated GSK 3Ser9 increased (P lt;0.05). Conclusions A1 40 PC12 cell injury induced by the process, there has been excessive tau protein phosphorylation, can Ser396, Ser199/202 sites and Tau 5 protein concentration. activate GSK 3 is to produce tau hyperphosphorylation of the main ways. MCI 186 can inhibit the activity of GSK 3, thereby reducing the A1 40-induced tau hyperphosphorylation, to achieve the purpose of protecting nerve cells.
[Keywords:] edaravone; Alzheimer’s disease; glycogen synthase kinase 3; tau protein phosphorylation
AD is a common neurodegenerative disease, in the pathogenesis of many more scholars tend to change the core of tau hyperphosphorylation. Current clinical drugs used to treat AD are only mild to moderate improvement some patients with symptoms, not alleviate the pathological changes in the brain to stop the progress of the disease, and hyperphosphorylation of tau protein did not reverse the effect. edaravone (MCI 186) is a free radical scavenger, can specifically scavenge hydroxyl radical (OH), secondary to inhibition of oxidative stress and apoptosis play a
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