PJ34对胸主动脉再灌注损伤小鼠模型脊髓组织活力和基因表达的影响。
Effect of PJ34 on spinal cord tissue viability and gene expression in a murine model of thoracic aortic reperfusion injury.
作者信息
Stone David H, Conrad Mark F, Albadawi Hassan, Entabi Fateh, Stoner Michael C, Cambria Richard P, Watkins Michael T
机构信息
Division of Vascular and Endovascular Surgery, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
出版信息
Vasc Endovascular Surg. 2009 Oct-Nov;43(5):444-51. doi: 10.1177/1538574409333582. Epub 2009 Jul 29.
INTRODUCTION
These studies were designed to determine whether PJ34, a novel Poly-ADP Ribose Polymerase Inhibitor, modulates expression of markers of stress and inflammation in the spinal cord following ischemia/ reperfusion(TAR).
METHODS
129S1/SvImj mice were subjected to thoracic aortic occlusion and 48 hours of reperfusion (n = 38). EXPERIMENTAL GROUPS INCLUDED: Untreated Control (UC, n = 21); PJ34 (PJ34, n = 11) and sham (S, n = 6). At 48 hours, mice were euthanized for mRNA analysis and assessment of spinal cord viability.
RESULTS
PJ34 improved spinal cord tissue viability following TAR (UC:53.1 +/- 6.3, PJ34:73.5 +/- 4.1% sham, p < 0.01). mRNA analysis revealed significant expression of stress response genes in UC and PJ34 treated mice.
CONCLUSIONS
PJ34 enhanced mitochondrial activity and preserved neurologic function following TAR despite the expression of stress and pro-inflammatory markers within the spinal cord. The ongoing cord stress response in neurologically intact PJ34 treated mice may indicate the potential to develop delayed neurologic dysfunction.
引言
这些研究旨在确定新型聚ADP核糖聚合酶抑制剂PJ34是否能调节脊髓在缺血/再灌注（TAR）后应激和炎症标志物的表达。
方法
对129S1/SvImj小鼠进行胸主动脉阻断并再灌注48小时（n = 38）。实验组包括：未治疗对照组（UC，n = 21）；PJ34组（PJ34，n = 11）和假手术组（S，n = 6）。48小时后，对小鼠实施安乐死以进行mRNA分析和评估脊髓活力。
结果
TAR后，PJ34改善了脊髓组织活力（UC组：53.1±6.3，PJ34组：73.5±4.1%，假手术组，p < 0.01）。mRNA分析显示，UC组和PJ34治疗组小鼠中应激反应基因有显著表达。
结论
尽管脊髓内存在应激和促炎标志物，但TAR后PJ34增强了线粒体活性并保留了神经功能。在神经功能完整的PJ34治疗小鼠中持续存在的脊髓应激反应可能表明有发生迟发性神经功能障碍的可能性。
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