The Kampo medicine Yokukansan (YKS) enhances nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells
| Autor: | Jiro Takata, Koji Chiba, Kazuki Terada, Atsushi Ishige, Yukari Matsushima, Kazuhisa Matsunaga, Yoshiharu Karube |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty animal structures neurite outgrowth Neurite Cell Survival Neuronal Outgrowth Yokukansan Tropomyosin receptor kinase A PC12 Cells Mice 03 medical and health sciences chemistry.chemical_compound Alzheimer Disease Neurotrophic factors Internal medicine Nerve Growth Factor Neurites medicine Animals Phosphorylation Receptor trkA Protein kinase B NGF lcsh:R5-920 Dose-Response Relationship Drug biology ERK1/2 business.industry Akt Cell Differentiation General Medicine Rats Kampo 030104 developmental biology Endocrinology Nerve growth factor chemistry nervous system biology.protein Medicine Kampo K252a business lcsh:Medicine (General) Drugs Chinese Herbal Signal Transduction Research Article Neurotrophin |
| Zdroj: | Bosnian Journal of Basic Medical Sciences, Vol 18, Iss 3 (2018) |
| ISSN: | 1840-4812 1512-8601 |
| Popis: | Accumulating evidence indicates that neurotrophic factor-like substances involved in the induction of neurotrophic factor synthesis may aid in the treatment of neurological disorders, such as Alzheimer’s disease. Yokukansan (YKS), a traditional Kampo medicine, has been used for the treatment of anxiety and mood disorders. In the present study, we aimed to identify the signaling pathways associated with YKS-mediated enhancement of nerve growth factor (NGF)-induced neurite extension in rat pheochromocytoma (PC12) cells. Akt and extracellular-regulated kinase 1/2 (ERK1/2) phosphorylation levels were assessed by western blot analysis, in the presence of YKS and following the treatment with TrkA inhibitor, K252a. YKS treatment (NGF+YKS 0.5 group) enhanced NGF-induced neurite outgrowth and phosphorylation/activation of Akt and ERK1/2 in PC12 cells. Moreover, YKS-induced effects were inhibited by the treatment with the TrkA receptor antagonist K252a (NGF+YKS 0.5+K252a group); no significant difference in neurite outgrowth was observed between K252a-treated (NGF+YKS 0.5+K252a group) and NGF-K252a-treated cells (NGF+K252a group). However, neurite outgrowth in K252a-treated cells (NGF+K252a and NGF+YKS 0.5+K252a group) reached only one-third of the level in NGF-treated cells (NGF group). NGF-mediated Akt phosphorylation increased by YKS was also inhibited by K252a treatment (NGF+YKS 0.5+K252a group), but no significant difference in ERK1/2 phosphorylation was observed between NGF-YKS-K252a- and NGF-treated cells (NGF group). Our results indicate that YKS treatment enhanced NGF-induced neurite outgrowth via induction of Akt and ERK1/2 phosphorylation, following the binding of NGF to the TrkA receptor. These findings may be useful in the development of novel therapeutic strategies for the treatment of Alzheimer’s disease. |
| Databáze: | OpenAIRE |
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