摘要
目的:观察龙牙楤木总皂苷、Mito KATP激活剂二氮嗪(DZ)、Mito KATP抑制剂5-羟基癸酸(5-HD)、龙牙+5-HD对大鼠缺血再灌注损伤(ischemia reperfusion injury,IRI)心肌线粒体细胞色素C和膜电位的影响,并探讨龙牙楤木总皂苷在减轻MIRI中的作用及其机制。方法:将60只雄性Wistar大鼠随机分为对照组(假手术组)、模型组、DZ组、5-HD组、龙牙组和龙牙+5-HD组,每组10只,建立Langendorff离体心脏灌流模型。对照组只穿线不结扎,以改良K-H液持续平衡灌流105分钟;其余5组均穿线结扎冠状动脉停灌30分钟,再分别以改良K-H液、DZ、5-HD、龙牙楤木总皂苷、龙牙+5-HD复灌75分钟(其中龙牙+5-HD组以5-HD复灌15分钟继以龙牙楤木总皂苷复灌60分钟)。提取线粒体,western-blot半定量测定线粒体内细胞色素C水平,荧光酶标仪测线粒体膜电位。结果:龙牙组线粒体细胞色素C释放减少,膜电位较高,与模型组、5-HD组、龙牙+5-HD组相比差异有统计学意义(P<0.05),与DZ组相比差异无统计学意义(P>0.05)。结论:龙牙楤木总皂苷在MIRI时起到保护作用,能减少MIRI时细胞色素C的释放,稳定线粒体膜电位,其作用可能与mito KATP的开放有关。
Objective： To observe the effects of aralosides, MitoKATP DZX, MitoKATP 5-HD, LongYa plus 5-HD on mitochondrial cytochrome C and membrane potential of IRI rat Cardiac muscle cells, and explore the function and mechanism of aralosides on relieving MIRI. Methods： All 60 male wister rats were randomly divided into the control group （ sham operation group）, the model group, DZ group, 5-HD group, aralosides group, aralosides plus 5-HD group, each group 10 rats, Langendorff reperfusion model in isolated heart was built. The control group was given threading, not ligation, persistent and balanced perfusion by improved K-H liquid for 105 min. The other five groups were given threading and ligation for coronary artery, perfusion stopped for 30 min, then reperfusion by improved K-H liquid, DZ, 5-HD, aralosides and aralosides plus 5-HD for 75 min （ the aralosides plus 5-HD group was reperfused for 15 min, also reperfused by aralosides for 60 min）. Mitochondria were extracted, mitochondrial cytochrome C was measured by western-blot semiquantitative analysis. Mitochondrial membrane potential was measured by microplate system. Results： The release of mitochondrial cytochrome C in aralosides group reduced, membrane potential increased, compared with the control group, 5-HD group and aralosides plus 5-HD group, there were statistical differences （P〈0.05）, compared with DZ group, there were no statistical differences （P〉0.05）. Conclusion： Aralosides can protect MIRI, reduce the release of mitochondrial cytochrome C in MIRI, stabilize mitochondrial membrane potential, its function might be related to MitoKATP open.
出处
《西部中医药》
2016年第12期9-12,共4页
Western Journal of Traditional Chinese Medicine
基金
国家自然科学基金课题(编号81273691)
