1. Effects of Ginkgolide A on Okadaic Acid-induced Tau Hyperphosphorylation and the PI3K-Akt Signaling Pathway in N2a Cells
- Author
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Tianlong Zhai, Jianhua Chen, Cunji Xu, Jian Pan, Yan Chen, Peilu Duan, Meili Hu, Cui Wang, and Jingna Ding
- Subjects
Cell Survival ,Pharmaceutical Science ,tau Proteins ,Cell Line ,Analytical Chemistry ,Lactones ,Mice ,Neuroblastoma ,Phosphatidylinositol 3-Kinases ,chemistry.chemical_compound ,Alzheimer Disease ,Okadaic Acid ,Drug Discovery ,Animals ,Viability assay ,Phosphorylation ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Pharmacology ,Plant Extracts ,Chemistry ,Organic Chemistry ,Ginkgo biloba ,Okadaic acid ,N2a cell ,Cell biology ,Ginkgolides ,Complementary and alternative medicine ,Biochemistry ,Molecular Medicine ,Signal transduction ,Intracellular ,Signal Transduction - Abstract
Alzheimer's disease is the most common form of dementia leading to the irreversible loss of neurons, and Tau hyperphosphorylation has an important role in the pathology of Alzheimer's disease. Ginkgolide A is one of the active components of Ginkgo biloba extracts which has been proven to have neuroprotective effects, but the effect of ginkgolide A on Tau hyperphosphorylation has not yet been reported. In this study, the effects of ginkgolide A on cell viability, Tau hyperphosphorylation, and the PI3K-Akt signaling pathway in N2a cell lines were explored, and methods such as the MTT assay, ELISA, and Western blots techniques were used. The results showed that ginkgolide A could increase cell viability and suppress the phosphorylation level of Tau in cell lysates, meanwhile, GSK3β was inhibited with phosphorylation at Ser9. Moreover, treatment of the cells with ginkgolide A promoted phosphorylation of PI3K and Akt, suggesting that the activation of the PI3K-Akt signaling pathway may be the mechanism for ginkgolide A to prevent the intracellular accumulation of p-Tau induced by okadaic acid and to protect the cells from Tau hyperphosphorylation-related toxicity.
- Published
- 2012