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Planta Med 2012; 78(12): 1337-1341
DOI: 10.1055/s-0032-1314965
Biological and Pharmacological Activities
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Effects of Ginkgolide A on Okadaic Acid-induced Tau Hyperphosphorylation and the PI3K-Akt Signaling Pathway in N2a Cells

Yan Chen
1   School of Life Science, Anhui University, Hefei, Anhui, China
,
Cui Wang
1   School of Life Science, Anhui University, Hefei, Anhui, China
,
Meili Hu
1   School of Life Science, Anhui University, Hefei, Anhui, China
,
Jian Pan
2   Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, Hefei, Anhui, China
,
Jianhua Chen
1   School of Life Science, Anhui University, Hefei, Anhui, China
,
Peilu Duan
1   School of Life Science, Anhui University, Hefei, Anhui, China
,
Tianlong Zhai
1   School of Life Science, Anhui University, Hefei, Anhui, China
,
Jingna Ding
1   School of Life Science, Anhui University, Hefei, Anhui, China
,
Cunji Xu
1   School of Life Science, Anhui University, Hefei, Anhui, China
› Author Affiliations
Further Information

Publication History

received 28 March 2012
revised 22 May 2012

accepted 23 May 2012

Publication Date:
14 June 2012 (online)

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Abstract

Alzheimerʼs 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 Alzheimerʼs 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.

Key words

ginkgolide A - Tau hyperphosphorylation - N2a cells - PI3K-Akt signaling pathway
 

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