Neuroprotective effect of pterostibene on oxygen- glucose deprivation/reperfusion injury and its mechanism in neurons

Objective To explore the protective effect of pterostibene (PTE) on oxygenglucose deprivation/reperfusion (OGD/R) injury and its mechanism in HT22 neurons. Methods The HT22 neurons of routine culture were divided into OGD/R group, PTE 1.25 μmol/L+ OGD/R group, PTE 2.5μmol/L+OGD/R group and PTE 5 μmol/L+OGD/R group. Cells in the later three groups were given different concentrations of PTE for 2 h; and then, cell from all the groups were induced OGD/R. Six h after that, cell viability was accessed by MTT assay, lactate dehydrogenase (LDH) release was detected with specific kit, intracelluar reactive oxygen species (ROS) levels were measured by non-fluorescent probe 2',7'-dichlorofluorescein diacetate (DCFH-DA), neuronal apoptosis was determined by TUNEL and Bax/Bcl-2 ratio was evaluated by Western blotting. Results As compared with the OGD/R group, PTE treatment groups had significantly increased cell viability and reduced LDH release, ROS level and apoptotic rate (P<0.05); the decreased/increased extents were PTE 1.25 μmol/L + OGD/R group<PTE 2.5 μmol/L+OGD/R group<PTE 5 μmol/L+OGD/R group, with significant differences (P< 0.05). PTE could also increased Bcl-2 expression and decreased Bax expression, and the Bax/Bcl-2 ratio in the OGD/R group, PTE 1.25 μmol/L+ OGD/R group, PTE 2.5 μmol/L+ OGD/R group and PTE 5 μmol/L+OGD/R group was decreased in sequence, with significant differences (P<0.05). Conclusion PTE can fight against ischemia reperfusion injury in neurons by suppression of cell apoptosis and ROS levels. Key words: Pterostibene; Oxygen- glucose deprivation/reperfusion model; HT22 neuron; Neuroprotection