Cerebral ischemia/reperfusion injury plays an important role in the development of tissue injury after acute stroke, including neutrophils adhesion and infiltration, inflammation and oxidative stress. 10-O-(N,N-dimethylaminoethyl)-ginkgolide B methanesulfonate (XQ-1H) is a novel ginkdolide B derivative. In this study, we investigated the anti-inflammatory and anti-oxidative activities of XQ-1H in vivo and vitro. In our study, rats were treating with XQ-1H (31.2, 15.6 and 7.8mg/kg) after middle cerebral artery occlusion surgery. Primary cultured cortical rat neurons were treated with Na2S2O4 for 1.5h to mimic hypoxia and reoxygenation injury in vitro. Cortical neurons were preincubated with XQ-1H (100, 10, 1μM) 24h before hypoxic injury. Brain edema was evaluated by brain water content. Neutrophil infiltration was determined by fluorescence imaging method and myeloperoxidase assay. Intercellular adhesion molecule 1 (ICAM-1) and matrix metallopeptidase 9 (MMP-9) expressions were examined by immunohistochemistry analysis. Neuronal injury was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide, lactate dehydrogenase releasing and lactic acid content. The anti-oxidative effects of XQ-1H were evaluated by superoxide dismutase (SOD) activity and malondialdehyde content in ischemic brain and neuron cultures subjected to hypoxia/reoxygenation procedure. Results showed that XQ-1H reduced neutrophils infiltration to ischemic brain, which might result from down regulation of inflammatory mediators, such as ICAM-1 and MMP-9. In addition, an antioxidative effect of XQ-1H was observed in cortical neuron and brain homogenates by enhancing SOD activity and inhibiting lipid peroxidation. These results indicated that XQ-1H possessed a protective effect against cerebral ischemia, especially on neutrophil infiltration and oxidative stress.