the effect of noscapine on oxygen-glucose deprivation on primary murine cortical neurons in high glucose condition

abstractin the present work we set out to investigate the neuroprotective effects of noscapine (0.5-2 µm) in presence of d-glucose on primary murine foetal cortical neurons after oxygen–glucose deprivation/24 hrs 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 pre-treatment. 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+]i induced by sodium azide/glucose deprivation (chemical ogd) model. these effects were more pronounced than that of 25 or 100 mm d-glucose alone.the present study demonstrated that the neuroprotective effects of hg after 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.