ABSTRACT
Objective To investigate the effect of resveratrol on oxidative stress of rat primary cortical neurons during different time windows of oxygen-glucose deprivation/reperfusion (0GD/RP) injury. Methods Rat cortical neurons were cultured under oxygen and glucose deprivation for 150 min and returned to normal culture for 24 h. The experiment was divided into 6 groups, including the normal group, model group, pre-treatment group (treated with resveratrol for 24 h prior to OGD), OGD-treatment group (treated with resveratrol during 150 min of 0GD and 24 h of reperfusion), post-treatment group(treated with resveratrol during 24 h of reperfusion), and thewhole processing group (treated with resveratrol for 24 h prior to 0GD, during 150 min of OGD, and 24 h ofreperfusion). Invert microscope was used to observe cell morphology. Chemical colorimetry was used to detect the activity of superoxide dismutase (SOD) and the content of nitric oxide (NO). Immunofluorescencewas used to detect the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2). Western blotting analysis was used reveal the the proteinexpressions of Nrf2, heme oxygenase-1 (HO-1) and NADP (H); quinone oxidoreductase-1 (NQO-1). Results The stereoscopic effect and refraction ofneurons were enhanced at the sixth day of culture. Compared with the model group, resveratrol of various concentrations (10, 20, 40, 60 and 80 μmol/L) significantly elevated the activity of SOD and decreased N0 content in the whole processing group (P<0.05) with the effect being the besttranslocation of Nrf2 from the cytoplasm into the nuclei and upregulated Nrf2, HO-1 and NQO-1 protein expression at all stages of OGD/RP injury, with thebest effect found in the whole processing group, followed by the pre-treatment group. Conclusion Resveratrol has a dose-dependent anti-oxidative stress effect on rat cortical neurons during OGD/RP injury, with the best effect seen in the whole processing group, followed by the pre-treatment group. The mechanism might be associated with activation of Nrf2/antioxidant response element (ARE) signaling pathway and the sbusequent upregulation of antioxidant protein expression.