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线粒体分裂抑制剂对大鼠急性脊髓损伤后线粒体形态与功能的影响 被引量:3

Effects of mitochondrial fission inhibitor on the mitochondrial morphology and function after acute spinal cord injury in rats
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摘要 目的 旨在检测选择性线粒体分裂抑制剂-1(Mdivi-1)预处理对大鼠急性脊髓损伤(ASCI)后线粒体形态,线粒体膜电位(MMP)及线粒体ATP含量的影响。方法 成年雌性SD大鼠72只,体重250~300 g,采用随机数字表法,将大鼠随机分为3组(n=24):假手术组(Sham组)、单纯脊髓损伤组(SCI组)和Mdivi-1预处理组(1.20 mg/kg,Mdivi-1组),每组24只。SCI组和Mdivi-1组大鼠采用Allen’s方法制备ASCI模型,Mdi-vi-1组和SCI组大鼠在脊髓打击之前15 min经尾静脉分别给予Mdivi-1或等容量二甲基亚砜(DMSO)。每组大鼠再分为两个亚组,分别于脊髓暴露或者打击后的3和12 h处死,取出脊髓T9-11,采用透射电子显微镜检测线粒体形态,用荧光显微镜和荧光分光光度计检测MMP变化,用荧光分光度计检测线粒体ATP含量的变化。结果 与Sham组相比,SCI 3 h组时,线粒体数目明显减少(〈0.01),截面积明显增大(〈0.01),但MMP和线粒体ATP含量无明显变化;SCI 12 h组时,线粒体数目明显增多(〈0.01),截面积明显减小(〈0.01),但MMP和线粒体ATP含量明显减低(〈0.01)。与SCI组相比,Mdivi-1 3 h组时,线粒体数目、截面积及MMP和线粒体ATP含量无明显变化;而Mdivi-1 12 h组时,线粒体数目明显减少(〈0.01),截面积明显增大(〈0.01),MMP和线粒体ATP含量明显升高(〈0.01)。结论 选择性线粒体分裂抑制剂-Mdivi-1能有效抑制ASCI后线粒体分裂和MMP降低,增加线粒体中ATP的合成,从而保护了线粒体功能。 [Objective] To detect the effect of selective mitochondrial fission inhibitor-Mdivi-1 on mitochondrial morphology, mitochondrial membrane potential and the content of mitochondrial ATP after acute spinal cord injury in rats. [Methods] 72 adult female SD rats , weighing 250-300 g, were randomly divided into 3 groups (n =24): sham operation group(Sham group), acute spinal cord injury group (SCI group), Mdivi-1 pretreatment group (1.20 rag/ kg, Mdivi-1 group) using a random number table. The Spinal cord injury model of rats in SCI group and Mdivi-1 group were made by Allen's method. In sham group, the rats were exposed, but not hit. In Mdivi-1 group, the rats were given Mdivi-1 15 rain before spinal cord injury through the tail vein, but SCI group received the same amount of dimethyl sulfoxide(DMSO). Each group was divided into two sub-groups. The rats were sacrificed at 3 h and 12 h respectively after exposing spinal cord or spinal cord injury, and then the spinal cord T9-11 was removed. Mitochon- drial morphology was detected by transmission electron microscopy. Mitochondrial membrane potential was detected by fluorescence microscope and fluorescence spectrophotometer. The content of mitochondrial ATP was detected by fluorescence spectrophotometer. [ Results ] Compared with Sham group, the number of mitochondria in SC1 3 h group reduced significantly (P 〈0.01) and cross-sectional area increased significantly (P 〈0.01), but no significant changes were found in mitoehondrial membrane potential and content of mitochondrial ATP; The number of mitochondria in the SCI group at 12 h increased significantly (P 〈0.01), but cross-sectional area, mitochondrial membrane potential and content of mitochondrial ATP reduced significantly (P 〈0.01). Compared with the SCI group, the number of mi- toehondria, cross-sectional area, mitochondrial membrane potential and content of mitochondrial ATP have no slgnif~ icant changes in the Mdivi-1 group at 3 h; However, the number of mitochond
出处 《中国现代医学杂志》 CAS 北大核心 2015年第1期1-6,共6页 China Journal of Modern Medicine
基金 国家自然科学基金(No:81272074) 辽宁省博士科研启动基金(No:20121094) 辽宁医学院校长基金(No:XZJJ20130204)
关键词 急性脊髓损伤 线粒体分裂抑制剂 线粒体形态 线粒体膜电位 三磷酸腺苷 acute spinal eord injury mitochondrial fission inhibitor mitochondrial morphology mitochondrial membrane potential adenosine triphosphate
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  • 1MCEWEN ML, SULLIVAN PG, RABCHEVSKY AG, et al. Targeting mitochondrial function for the treatment of acute spinal cord injury[J]. Neurotherapeutics, 2011, 8(2): 168-179. 被引量:1
  • 2WESTERMANN B. Mitochondrial fusion and fission in cell life and death[J]. Nat Rev Mol Cell Biol, 2010, 11(12): 872-884. 被引量:1
  • 3KOCH A, YOON Y, BONEKAMP NA, et al. A role for fisl in both mi- toehondrial and peroxisomal fission in mammalian cells [J]. Mol Biol Cell, 2005, 16(11): 5077-5086. 被引量:1
  • 4GAZARYAN IG, BROWN AM. Intersection between mitochondrial permeability pores and mitochondrial fusion/fission[J]. Neurochem Res, 2007, 32(4-5): 917-929. 被引量:1
  • 5KROEMER G, ZAMZAMI N, SUSIN SA. Mitoehondrial control of apoptosis[J]. Immunol Today, 1997, 18(1): 44-51. 被引量:1
  • 6CAO Y, LV G, WANG YS, et al. Mitochondrial fusion mad fission after spinal sacord injury in rats[J]. Brain Res, 2013, 1522: 59-66. 被引量:1
  • 7LACKNER LL, NUNNARI J. Small molecule inhibitors of mitochon-drial division: Tools that translate basic biological research into medicine[J]. Chem Biol, 2010, 17(6): 578-583. 被引量:1
  • 8ALLEN A. Surgery of experimental lesions of spinal cord equivalent to crush injury of fracture dislocation of spinal column : a preliminary re- port[J]. J Am Med Assoc, 1911, 57: 878-880. 被引量:1
  • 9HAN X, LU M, WANG S, et al. Targeting ikk/nf-kappab pathway re- duces infiltration of inflammatory cells and apoptosis after spinal cord iniury in rats[J1. Neurosci Lett, 2012, 511(1~: 28-32. 被引量:1
  • 10SHEN X, ZHENG, S, THONGBOONKERD, V, et al. Cardiac mito- chondrial damage and biogenesis in a chronic model of type 1 diabetes [J]. Am J Physiol Endoc.rinol Metab, 2004, 287: E896-E905. 被引量:1

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