1Department of Pathology, 2Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, China

Abstract 

Objective To determine whether sulforaphane (SFN) protects neurons against injury caused by oxygenglucose deprivation/reoxygenation (OGD/R) and, if so, to investigate the possible mechanisms. Methods Primary cultures of neurons were prepared from the cerebral cortex of 1-day-old Sprague-Dawley rats. On days 5–6 in vitro, the neurons were exposed to OGD for 1 h, followed by reoxygenation for 24 h. Cells were treated with 0, 0.1, 0.2, 0.5, 1, 2.5, or 5 μmol/L SFN, with or without 10 μmol/L LY294002, a PI3K-specific inhibitor, during OGD/R (a total of 25 h). After 24-h reoxygenation,MTT was used to assess viability and injury was assessed by Hoechst 33258/propidium iodide (PI) staining; immunofluorescence staining and Western blot were performed to detect molecular events associated with apoptosis. Results The MTT assay showed that 1 μmol/L SFN significantly increased viability, and Hoechst 33258/PI staining showed that the numbers of injured neurons were reduced significantly in the SFN group. Furthermore, immunofluorescence staining and Western blot showed that SFN increased Bcl-2 and decreased cleaved caspase-3 levels. Moreover, LY294002 inhibited the phosphorylated-Akt expression evoked by SFN, decreased Bcl-2 expression and increased cleaved caspase-3 expression. Conclusion SFN protects neurons against injury from OGD/R and this effect may be partly associated with an antiapoptosis pathway.

Keywords

sulforaphane; oxygen-glucose deprivation; apoptosis; neuroprotection

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