乌司他丁减轻失血性休克神经元线粒体功能障碍的临床观察

Clinical observation on protective effect of Ulinastatin against hemorrhagic shock-induced neuron mitochondrial dysfunction

目的探讨乌司他丁对失血性休克诱导的神经元线粒体功能障碍的影响。方法18只大鼠随机分为对照组、休克＋生理盐水组和休克＋乌司他丁组，在失血性休克造模后相应予以生理盐水或乌司他丁治疗。透射电镜检测神经元线粒体超微结构；JC-1探针流式细胞仪探测线粒体膜电位（△ψm）变化；荧光素-荧光素酶试剂盒测定ATP含量；过氧化脂质（lipid hydroperoxide，LPO）试剂盒检测血清LPO含量。结果与对照组比较，生理盐水组神经元线粒体肿胀、嵴结构模糊消失，低线粒体膜电位神经元比例增加（P〈0．05），神经元ATP含量降低（P〈0．05），血清LPO水平显著增加（P〈0．05）；而在乌司他丁处理组中以上改变均得到明显改善（P〈0．05）。结论乌司他丁通过抑制氧化应激而减少失血性休克诱导的神经元线粒体损伤，改善线粒体功能。

Objective To investigate protective effect of Ulinastatin on hemorrhagic shock-induced neuron mitochondrial dysfunction. Methods 18 rats were randomly divided into control group, shock＋normal saline （NS） group and shock＋Ulinastatin group. Rats were received homologous NS or Ulinastatin treatment after hemorrhagic shock induction. Uhrastructure of neuron mitochondria was detected by electron microscope; change of mitochondrial membrane potential （ △ψm） by JC-1 mitochondrial membrane potential kit; content of ATP by fluorescein-luciferase assay kit; lipid hydroperoxide （LPO） in serum by LPO assay kit. Results Compared with control group, mitochondrial swelling with poorly defined cristas, remarkably increased number of platelets with low mitochondrial membrane potential （ △ψm） （P 〈 0.05）, decreased ATP content （P 〈 0.05）, and increased serum LPO level （P 〈 0.05） were detected in NS group. These alterations mentioned were marked improved by Ulinastatin treatment （P 〈 0.05）. Conclusion Ulinastatin treatment can improve hemorrhagic shock-induced neuron mitochondrial injury and dysfunction via depression oxidative stress.