Effect of Tenuifoliside A isolated from Polygala tenuifolia on the ERK and PI3K pathways in C6 glioma cells
| Autor: | Ping Liu, Li-Hua Mu, Yuan Hu, Xian-Zhe Dong, Cui-li Huang, Bing-Ying Yu |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
MAPK/ERK pathway
Polygala Cell Survival MAP Kinase Signaling System Morpholines Carbazoles Pharmaceutical Science Tropomyosin receptor kinase B Biology CREB Disaccharidases Models Biological Plant Roots Indole Alkaloids Phosphatidylinositol 3-Kinases Cell Line Tumor Drug Discovery Nitriles Butadienes Animals Receptor trkB Viability assay Enzyme Inhibitors Phosphorylation PI3K/AKT/mTOR pathway Cell Proliferation Phosphoinositide-3 Kinase Inhibitors Pharmacology Brain-Derived Neurotrophic Factor biology.organism_classification CREB-Binding Protein Cell biology Rats Complementary and alternative medicine Chromones Polygala tenuifolia Cancer research biology.protein Molecular Medicine Signal transduction Drugs Chinese Herbal Signal Transduction |
| Zdroj: | Phytomedicine : international journal of phytotherapy and phytopharmacology. 21(10) |
| ISSN: | 1618-095X |
| Popis: | Tenuifoliside A (TFSA) is a bioactive oligosaccharide ester component of Polygala tenuifolia Wild, a traditional Chinese medicine which was used to manage mental disorders effectively. The neuroprotective and anti-apoptotic effects of TFSA have been demonstrated in our previous studies. The present work was designed to study the molecular mechanism of TFSA on promoting the viability of rat glioma cells C6. We exposed C6 cells to TFSA (or combined with ERK, PI3K and TrkB inhibitors) to examine the effects of TFSA on the cell viability and the expression and phosphorylation of key proteins in the ERK and PI3K signaling pathway. TFSA increased levels of phospho-ERK and phospho-Akt, enhanced release of BDNF, which were blocked by ERK and PI3K inhibitors, respectively (U0126 and LY294002). Moreover, the TFSA caused the enhanced phosphorylation of cyclic AMP response element binding protein (CREB) at Ser133 site, the effect was revoked by U0126, LY294002 and K252a. Furthermore, when C6 cells were pretreated with K252a, a TrkB antagonist, known to significantly inhibit the activity of brain-derived neurotrophic factor (BDNF), blocked the levels of phospho-ERK, phospho-Akt and phosphor-CREB. Taking these results together, we suggested the neuroprotection of TFSA might be mediated through BDNF/TrkB-ERK/PI3K-CREB signaling pathway in C6 glioma cells. |
| Databáze: | OpenAIRE |
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