Protection of Vitexin against Cerebral Ischemia-reperfusion Injury in Mice and the Mechanism

In this study, the protection of vitexin against cerebral ischemia-reperfusion injury (CIRI) in mice and the mechanism were investigated. Ninety mice were randomly divided into control, model and 10, 20, and 40 mg/kg vitexin groups, 18 mice in each group. The latter three groups were administrated with 10, 20, and 40 mg/kg vitexin, respectively, for seven days. Then, the CIRI model was established in the latter four groups. After 24 h from the modeling, compared with model group, in 20 and 40 mg/kg vitexin groups, the neurological deficit score, cerebral water content, and cerebral infarction range were significantly decreased, the brain tissue superoxide dismutase and glutathione peroxidase levels were significantly increased, the brain tissue malondialdehyde level was significantly decreased, the brain tissue tumor necrosis factor alpha, interleukin 1 beta, and intercellular cell adhesion molecule-1 levels were significantly decreased, the brain tissue nuclear factor kappa-B (NF-kappa B) p65 protein expression level was significantly decreased, and the brain tissue inhibitor of nuclear factor kappa-B alpha (I kappa B alpha) protein expression level was significantly increased (all P < 0.05). Above findings demonstrate that, the vitexin treatment may mitigate the CIRI in mice by decreasing the oxidative stress, reducing the inflammatory response and regulating the NF-kappa B/I kappa Ba signaling pathway.