Selegiline and Desmethylselegiline Stimulate NGF, BDNF, and GDNF Synthesis in Cultured Mouse Astrocytes
Autor: | Kyozo Hayashi, Ikuko Mizuta, Eiji Mizuta, Kiyoe Ohta, Mitsuhiro Ohta, Sadako Kuno, Masataka Nishimura |
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Rok vydání: | 2000 |
Předmět: |
medicine.medical_specialty
Monoamine Oxidase Inhibitors Parkinson's disease Biophysics Nerve Tissue Proteins Stimulation Endogeny Biochemistry Neuroprotection Mice Neurotrophic factors Internal medicine Nerve Growth Factor Selegiline Glial cell line-derived neurotrophic factor medicine Animals Glial Cell Line-Derived Neurotrophic Factor Nerve Growth Factors Molecular Biology Cells Cultured Mice Inbred ICR biology Chemistry Brain-Derived Neurotrophic Factor Amphetamines Cell Biology medicine.disease Nerve growth factor Endocrinology nervous system Astrocytes biology.protein medicine.drug |
Zdroj: | Biochemical and Biophysical Research Communications. 279:751-755 |
ISSN: | 0006-291X |
Popis: | We investigated the effects of selegiline and desmethylselegiline on synthesis of neurotrophic factors in cultured mouse astrocytes. Treatment with 2 mM selegiline for 24 h increased the contents of NGF, BDNF, and GDNF in the culture medium 26-, 1.7-, and 4.2-fold over the control, respectively. With this drug the maximum relative mRNA levels of NGF, BDNF, and GDNF were 6.2-fold at 2 h, 3.4-fold at 6 h, and 2.7-fold at 2 h, respectively. Selegiline at 0.2 mM completely inhibited the MAO activity, but had no effect on the content of neurotrophic factors, suggesting that stimulation of neurotrophic factors by selegiline is independent of MAO-B inhibition. Desmethylselegiline at 1.68 mM for 24 h elevated the NGF, BDNF, and GDNF contents 4.1-, 1.7-, and 2.4-fold over the control, respectively; and the relative transcript levels of NGF, BDNF, and GDNF reached 2.6-fold at 2 h, 1.7-fold at 6 h, and 1.8-fold at 2 h, respectively. These findings suggest that selegiline and desmethylselegiline may protect neurons by up-regulating endogenous NGF, BDNF, and GDNF synthesis. |
Databáze: | OpenAIRE |
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