枸杞多糖对小鼠脑缺血再灌注损伤的保护作用及其抗氧化应激的机制研究

目的探讨枸杞多糖(lycium barbarum polysaccharides,LBP)对缺血再灌脑损伤小鼠的保护作用及其可能的机制。方法通过颈总动脉栓线造成大脑中动脉缺血,缺血2 h后将栓线拔出以实现大脑中动脉血流再灌注,形成小鼠短暂性大脑中动脉阻塞(transient middle cerebral artery occlusion,t MCAO)模型,观察LBP(25 mg/kg,50 mg/kg和100 mg/kg)对小鼠脑梗死范围,脑含水量,神经症状的影响,采用Westernblot法检测缺血大脑皮质NOX4蛋白的表达,采用DHE染色法检测脑组织中ROS的生成,采用分光光度计检测缺血侧脑组织匀浆SOD活力,GSH-Px活力,及MDA含量。结果 LBP对缺血再灌注小鼠神经症状有明显的改善作用,能明显降低脑梗死范围和脑含水量。Westernblot结果显示:小鼠缺血再灌后,缺血侧大脑皮质NOX4蛋白水平明显增高,LBP能显著降低NOX4蛋白水平。DHE染色显示,LBP能显著降低缺血再灌后ROS的生成。LBP能升高SOD和GSH-Px活力,降低MDA含量。结论 LBP对缺血再灌注小鼠脑损伤有明显保护作用,该作用可能与其抑制脑缺血再灌注引起的氧化应激损伤有关。

Neuroprotection of LBP on a mouse model of transient focal cerebral ischemia and its protective mechanisms of in-hibiting oxidative stress

Objective To observe the protective effects of lycium barbarum polysaccharides (LBP) on cerebral is-chemia-reperfusion injury in mice and explore its mechanism.Methods Cerebral ischemia-reperfusion injury in mice was induced by middle cerebral artery occlusion.The neurological outcome,infarct size and water contents were evaluated. Western blotting was used to evaluate the protein levels of NOX4.DHE staining was used to evaluate levels of ROS.SOD and GSH-Px activity,MDA levels of ischemia cerebral tissue were determined by spectrophotometry using commercial kits. Results LBP markedly improved neurologic deficits,and decreased infarct size and edema at 24 h after reperfusion in mice.Western blot analysis indicated that LBP markedly down-regulated the protein level of NOX4.DHE staining indicated that LBP decreased the levels of ROS in ischemic cortex 24 h after reperfusion.SOD activity and GSH-Px activity in LBP groups was higher,and MDA level in LBP groups were significantly lower than those in vehicle group.Conclusion LBP has protective effects on cerebral ischemia-reperfusion injury in mice,and this effect may be associated with inhibiting oxi-dative stress induced by cerebral ischemia-reperfusion.