| 引用本文:黄志英1,2，孙文利2,3，张晓旭2,3，陈畅2，吴传鸿4，高健2，段飞鹏5，田朋朋2，3，李韶菁2，颜天华1.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[J].世界中医药,2015,10(03):. |
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| 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 |
| The Effects of Galangin on Mitochondrial Metabolism-related ATPases in Ischemic Stroke Rats |
| 投稿时间：2014-11-13 |
| DOI：10.3969/j.issn.1673-7202.2015.03.024 |
| 中文关键词: 高良姜素 缺血性脑卒中 线粒体 能量代谢 Na+-K+ATP酶 Ca2+-Mg2+ATP酶 |
| English Keywords:Galangin Ischemic stroke Mitochondrion Energy metabolism Na+-K+ATPase Ca2+-Mg2+ATPase |
| 基金项目:国家自然科学基金项目(编号：81274133,81303261),国家科技重大专项(重大新药创制)资助项目(编号：2012ZX09103201-055),中国中医科学院自主选题项目(ZZ2014005，ZZ2014060) |
| 作者 | 单位 | | 黄志英1,2，孙文利2,3，张晓旭2,3，陈畅2，吴传鸿4，高健2，段飞鹏5，田朋朋2，3，李韶菁2，颜天华1 | 1 中国药科大学药学院,南京,211198
2 中国中医科学院中药研究所,北京100700
3 河北大学药学院,保定,071002
4 澳门大学中华医药研究院中药质量研究国家重点实验室,澳门,999078
5 北京中医药大学中药学院,北京,100102 |
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| 中文摘要: |
| 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。 |
| English Summary: |
| 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 energy metabolism disorder. Methods: A total of 120 adult male Sprague–Dawley rats were randomly divided into 2 groups: preoperative 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. Neurological 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. Results: 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-1and 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. Conclusion: Galangin can improve the activity of Na+-K+ATPase and Ca2+-Mg2+ATPase significantly in rats impaired by middle cerebral 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. |
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