Effects of fluvoxamine on nerve growth factor-induced neurite outgrowth inhibition by dexamethasone in PC12 cells |
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Authors: | Yukari Matsushima Kazuki Terada Jiro Takata Yoshiharu Karube Chiaki Kamei |
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Affiliation: | 1. Faculty of Pharmaceutical Sciences, Department of Pharmacology, Yasuda Women’s University, Hiroshima, Japan;2. Faculty of Pharmaceutical Sciences, Department of Kampo and Natural Product Chemistry, Yokohama University of Pharmacy, Yokohama, Japan;3. Faculty of Pharmaceutical Sciences, Laboratory of Drug Design and Drug Delivery, Fukuoka University, Fukuoka, Japan |
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Abstract: | In the present study, we examined the effects of fluvoxamine on nerve growth factor (NGF)-induced neurite outgrowth inhibition by dexamethasone (DEX) in PC12 cells. Fluvoxamine increased NGF-induced neurite outgrowth. Compared with co-treatment with NGF and fluvoxamine, p-Akt levels were higher than the values without fluvoxamine. The phosphorylated extracellular regulated kinase 1/2 levels were slightly increased by co-treatment with NGF and fluvoxamine. Fluvoxamine concentration-dependently improved NGF-induced neurite outgrowth inhibition by DEX. Fluvoxamine also improved the decrease in the NGF-induced p-Akt level caused by DEX. Interestingly, the sigma-1 receptor antagonist NE-100 blocked the improvement effects of fluvoxamine on NGF-induced neurite outgrowth inhibition by DEX. The selective sigma-1 receptor agonist PRE-084 also improved NGF-induced neurite outgrowth inhibition by DEX, which is blocked by NE-100. These results indicate that the improvement effects of fluvoxamine on NGF-induced neurite outgrowth inhibition by DEX may be attributable to the phosphorylation of Akt and the sigma-1 receptor. |
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Keywords: | Nerve growth factor (NGF) neurite outgrowth fluvoxamine phosphorylated Akt dexamethasone (DEX) |
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