高良姜素对缺血性脑卒中大鼠脑线粒体代谢相关酶的影响

摘要

目的：观察高良姜素对缺血性脑卒中大鼠脑线粒体能量代谢相关 ATP 酶的影响，探讨高良姜素通过干预线粒体能量代谢障碍发挥缺血性脑卒中保护作用的可能机制。方法：将120只雄性 SD 大鼠随机分成两大组，即术前给药组和术后给药组，每大组中又分为假手术组、模型组、阳性药银杏叶提取物 EGb761组（mg·kg －1）及高良姜素高、中、低剂量组（100，50，25 mg·kg －1），每组10只。大鼠行中动脉栓塞手术前15 min 或者术后6 h 灌胃给药或给予等量生理盐水，于手术后24 h 进行神经功能学评分，制备缺血侧脑组织线粒体悬液，并对其 Na ＋-K ＋ATP 酶，Ca2＋-ATP 酶，Mg2＋-ATP 酶，Ca2＋-Mg2＋ATP 酶活性进行检测。结果：高良姜素中剂量和高剂量组，Na ＋-K ＋ATP 和 Ca2＋-Mg2＋ATP 酶活性均有明显提高（P ＜0.05），低剂量组酶活性无明显改变；相比较，Ca2＋-ATP 酶，Mg2＋-ATP 酶活性各组之间没有明显的差别。结论：高良姜素能明显提高缺血性脑卒中大鼠脑线粒体 Na ＋-K ＋ATP 酶和 Ca2＋-Mg2＋ATP 酶活性，缓解缺血脑细胞的能量代谢障碍，是其发挥脑缺血保护作用的可能机制之一。%Objective:To clarify the effects of galangin on mitochondrial energy metabolism-related ATPases in ischemic stroke rats,and to explore the possible protective mechanisms of ganlangin on ischemic stroke through intervening the mitochondrial ener-gy metabolism disorder.Methods:A total of 120 adult male Sprague Dawley rats were randomly divided into 2 groups:preoper-ative and postoperative treatment group.Each group (n =10 /group)was also divided into 6 groups:sham group,vehicle group, positive control EGb761 group (4 mg·kg -1 )and galangin-treated groups (100,50 and 25 mg·kg -1 ).Galangin,EGb761 and physiological saline were administered by intragastric administration(i.g.)15 min prior to MCAO or 6 h after MCAO.Neurologi-cal deficit scores were determined at 24 h after MCAO.The crude mitochondria of the ischemic brain tissue was prepared followed by the assay for the activity of the mitochondrial Na +-K +ATPase,Ca2 +-ATPase,Mg2 +-ATPase and Ca2 +-Mg2 +ATPase.Re-sults:The activity of Na +-K +ATPase and Ca2 +-Mg2 +ATPase was significantly improved (P <0.05)in the groups treated with EGb761 and galangin (50 mg·kg -1 and 100 mg·kg -1 )and the activity in the groups treated with galangin (25 mg·kg -1 )did not change significantly.The activity of Ca2 +-ATPase and Mg2 +-ATPase had no significant differences among all the groups.Con-clusion:Galangin can improve the activity of Na +-K +ATPase and Ca2 +-Mg2 +ATPase significantly in rats impaired by middle cer-ebral artery occlusion (MCAO)-induced ischemic stroke,relieving the energy metabolic disorder of brain cell.It might be one of the therapeutic mechanisms of ganlangin on ischemic stroke.