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The effect of noscapine on oxygen-glucose deprivation on primary murine cortical neurons in high glucose condition
Authors
S.-A. Ebrahimi
M. Mahmoudian
N. Rahbar-Roshandel
G. Vahabzadeh
Publication date
1 January 2016
Publisher
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on
PubMed
Abstract
In the present work we set out to investigate the neuroprotective effects of noscapine (0.52 µM) in presence of D-glucose on primary murine foetal cortical neurons after oxygen� glucose deprivation/24 h. recovery. Cell viability, nitric oxide production and intracellular calcium ((ca2+)i) levels were evaluated by MTT assay, the modified Griess method and Fura-2 respectively. 25 and 100 mM D-glucose could, in a concentration dependent manner, improve cell viability and decrease NO production and (ca2+)i level in neuronal cells after ischemic insult. Moreover, pre-incubation of cells with noscapine, noticeably enhanced protective effects of 25 and 100 mM D-glucose compared to similar conditions without noscapine pretreatment. In fact, noscapine attenuated NO production in a dose-dependent fashion, after 30 minutes (min) OGD, during high-glucose (HG) condition in cortical neurons. Pretreatment with 2 μM noscapine and 25 or 100 mM D-glucose, was shown to decrease the rise in (ca2+) induced by Sodium azide/glucose deprivation (chemical OGD) model. These effects were morei pronounced than that of 25 or 100 mM D-glucose alone. The present study demonstrated that the neuroprotective effects of HG before an ischemic insult were augmented by pre-treatment with noscapine. Our results also suggested that the neuroprotection offered by both HG and noscapine involve attenuation of NO production and (ca2+)i levels stimulated by the experimental ischemia in cortical neurons. © 2016 by School of Pharmacy
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eprints Iran University of Medical Sciences
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Last time updated on 10/10/2019