Neuroprotective effect and signal transduction mechanisms of sodium ferulate on oxygen-glucose deprivation injured cultured mouse cortical astrocytes

Objective: To investigate the protective effect and mechanism of sodium ferulate(SF) on oxygen-glucose deprivation(OGD)-inducing injury in astrocytes in vitro. Methods: Primary cultured astrocytes were divide into 7 groups: the control group,OGD group,OGD + SF(50,100,200 mol/L) groups,SB 203580 group,OGD + SB 203580 group. Cultured astrocytes were pretreated with or without SF for 24 h or SB203580 for 1 h,then,astrocytes were exposed to 6 h oxygen glucose deprivation(OGD) and the cell injury were evaluated by the morphology changes,the cell viability,the apoptosis and LDH leakage. The astrocyte apoptosis was quantified by scoring the percentage of cells with apoptotic nuclear morphology after Hoechst 33258 staining. Protein expressions of active caspase-3 and phosphorylated P38 were measured by western blot. In order to investigate the mechanism responsible for protective effects of SF,SB203580 was added to cells 1 h prior to OGD treatment. Results: After astrocytes were exposed to 6 h OGD,compared with the control,cells were the vacuolization,and the cell viability was decreased,the LDH leakage of astrocytes was increased. Cells were induced to undergo apoptosis as evidenced by nuclear shrinkage,and the percentage of apoptotic cells was increased. OGD also induced the increase in phosphorylated P38 and active caspase-3 expression by western blot. SF(50,100,200 μmol/L) reduced OGD-evoked apoptotic morphology,active caspase-3 expression and increased the cell viability and decreased LDH leakage in cultured astrocytes. Further,SF inhibited OGD-inducing the phosphorylation of P38,and active caspase-3 expression. Conclution: SF prevents OGD-inducing injury through suppression of p38 MAPK signal pathway in cultured astrocytes.