Noscapine Modulates Neuronal Response to Oxygen-glucoseDeprivation/Reperfusion Injury Via Activation of Sigma-1Receptor in Primary Cortical Cultures

In the present study, we investigated the effects of noscapine (0.5-2 μm), an alkaloid fromthe opium poppy (papaver somniferum), on primary murine cortical neurons exposed to 60min oxygen–glucose deprivation (ogd) in the presence of 5 μm bd-1047, a selective sigma-1receptor antagonist. the experiments were performed on cortical neurons after 11–16 days ofculture. to initiate oxygen–glucose deprivation, the culture medium was transferred to glucosefreedmem, and placed in a humidified incubation chamber containing a mixture of 95% n2 and5% co2 at 37 °c for 60 min. in order to explore the effect on neurons under oxygen–glucosedeprivation in this condition, some cultures were pretreated with noscapine and bd1047 together,24 h prior to ogd followed by 24 h recovery. cell viability, nitric oxide (no) production andintracellular calcium concentration ([ca2+]i) levels were evaluated by mtt assay, the modifiedgriess method, and fura-2, respectively. pretreatment of the cultures with noscapine in thepresence of bd1047 significantly increased cell viability and decreased no generation in a dosedependentmanner compared to bd1047 alone. pretreatment with 2 μm noscapine and bd-1047 was shown to decrease the rise in [ca^2+]i induced by sodium azide (nan3) and glucose deprivation.we concluded that noscapine in the presence of bd1047 could protect primary cortical neuronsafter oxygen–glucose deprivation-induced cell injury but this effect was not complete. our resultsindicate that neuroprotective effects of noscapine could be mediated partially through activationof sigma-1 receptor and by decreasing no production and [ca^2+]i levels.