二氮嗪对心肺复苏后脑线粒体的影响

发布时间：2018-04-10 00:35

本文选题：心肺复苏　切入点：脑损伤　出处：《中山大学学报(医学科学版)》2016年05期

【摘要】：【目的】探讨二氮嗪能否通过开放线粒体ATP敏感性钾通道(mito KATP)起到抗氧化应激和保护线粒体的结构和功能,减轻缺血再灌注引起的脑细胞损伤。【方法】经窒息诱导的心脏停搏(CA)和心肺复苏(CPR)成功的雄性SpragueDawley(SD)大鼠24只,恢复自主循环(ROSC)后30 min,用抽签法随机分为3组,每组8只,分别为载体(Vehicle)组:给予0.1mol/L二甲基亚砜(DMSO)1 m L腹腔注射;二氮嗪(DZ)组:给予DZ(10 mg/kg)腹腔注射(DZ溶解在0.1 mol/L DMSO 1 m L中,下组相同);DZ+5-羟基癸酸盐(DZ+5-HD)组:给予DZ(10 mg/kg)腹腔注射,同时给予5-HD(5 mg/kg)腹腔注射。另设假手术组(Sham)5只。手术后或复苏后24 h处死各组动物,取脑皮质进行丙二醛(MDA)、活性氧族(ROS)和超氧化物歧化酶2(SOD2)检测,提取线粒体测定呼吸控制率(RCR)和用电子显微镜观察脑皮质超微结构。【结果】复苏后24 h脑组织MDA和ROS浓度升高,SOD2活性下降,RCR下降,线粒体结构出现损坏;DZ干预后MDA和ROS浓度下降,SOD2活性上升,RCR上升,线粒体结构得到保护;但经5-HD共同干预后DZ的保护作用被取消。【结论】DZ通过开放mito KATP通道可起到抗氧化应激损伤、保护线粒体结构和功能的作用,减轻复苏后脑损伤。
[Abstract]:[objective] to investigate whether diazazine can protect the structure and function of mitochondria by opening the sensitive potassium channel of mitochondrial ATP to KATP.[methods] Twenty-four successful male Sprague-Dawley SD rats induced by asphyxia and cardiopulmonary resuscitation (CPR) were divided into 3 groups by drawing lots at 30 min after recovery of autonomic circulation.The carrier vehicle group was given 0.1mol/L dimethyl sulfoxide DMSO1 mL intraperitoneal injection, and the diazazine DZ group was given DZ(10 mg / kg intraperitoneally to dissolve the DZ in 0.1 mol/L DMSO 1 mL, and the lower group was treated with DZ(10 mg / kg, the same DZ 5-hydroxydecanoate DZ 5-HDD) group was injected intraperitoneally with DZ(10 mg / kg.5-HD(5 mg / kg was also given intraperitoneally.The sham-operated group (5 rats) was set up.After operation or 24 hours after resuscitation, the animals in each group were killed, and the cerebral cortex was taken for the detection of malondialdehyde (MDA), reactive oxygen species (Ros) and superoxide dismutase (2SOD2).Mitochondria were extracted to measure respiratory control rate (RCR) and ultrastructure of cerebral cortex were observed by electron microscope. [results] after 24 hours of resuscitation, the concentration of MDA and ROS in brain tissue increased and the activity of SOD2 decreased.The concentration of MDA and ROS decreased and the activity of SOD2 increased, and the mitochondrial structure was protected.However, the protective effect of DZ was cancelled after the co-intervention of 5-HD. [conclusion] DZ can protect the structure and function of mitochondria by opening the mito KATP channel, protect the structure and function of mitochondria, and alleviate the brain injury after resuscitation.
【作者单位】：中山大学孙逸仙纪念医院急诊科/中山大学心肺脑复苏研究所;南海狮山华立医院;
【基金】：广东省科技计划社会发展项目(2012B031800084,2014A020212624)
【分类号】：R459.7

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