脊髓缺血损伤合并脓毒症后脊髓ZnT1表达的研究

目的：研究脊髓缺血损伤合并脓毒血症后大鼠脊髓的病理改变及脊髓组织中锌转运体1（zinc transporter1,ZnT1）的表达规律。方法：将32只wistar大鼠随机分为假手术组（s组，n=8）、腹主动脉阻断组（I／R组，n=8）、内毒素组（LPS组，n=8）和腹主动脉阻断＋内毒素组（I／R＋LPS组，n=8）。用HE染色的方法检测脊髓组织病理损害，用免疫组织化学的方法检测脊髓组织中ZnTl的表达规律。结果：1．病理结果改变：除S组外，I／R组、LPS组、UR＋LPS组三组大鼠HE染色切片中均可见脊髓组织损伤，各组脊髓损伤的严重程度有以下规律：S组〈I/R组〈LPS组〈I／R＋LPS组。2．免疫组化结果：脊髓损伤组ZnT1的表达较假手术组均增加（P〈0．05）。结论：1．脊髓缺血损伤合并内毒素攻击可导致严重的脊髓损伤。2．腹主动脉阻断合并内毒素攻击所致脊髓损伤早期脊髓组织中ZnT1表达上调，可能通过调节脊髓损伤早期脊髓组织中锌稳态平衡进而在脊髓损伤后脊髓神经元的病理生理活动中发挥重要作用，这一实验结果可为寻找早期脊髓损伤预防措施提供新的思路。

The Expression of Zinc Transporter 1 Following Spinal Cord Ischemia Injury and Subsequent Endotoxemia

Objective： To investigate the pathology change and the expression of zinc transporter 1 of rat spinal cord following spinal cord ischemia injury and subsequent endotoxemia. Methods： A total of 32 wistar rats were randomly and evenly divided into four groups： Sham group（S group,n=8）, Spinal cord ischemia-reperfusion group（I/R group,n=8）, Lipopolysaccharides group（LPS group,n=8） and Spinal cord ischemia-reperfusion plus Lipopolysaccharides group （I/R＋LPS group,n=8）. In spinal cord, hematoxylin and eosin stain- ing were used to examine the pathology change,immunohistochemistry（IHC） was used to measure the expression law ofZnT1. Results： 1. the pathology change： it could be observed spinal cord injury obviously in I/R group, LPS group and I/R＋LPS group. But there were some law among them. The degree of spinal cord injury in I/R＋LPS group and LPS group were serious than S group and//R group. The UR group was serious than S group. The I/R＋LPS group was serious than LPS group.2.Immunohistochemistry： The expression of ZnT1 in spinal cord injury groups were higher than that in sham group. Conclusion： 1.Abdominal aorta occlusion and subsequent endotoxemia can cause serious spinal cord injury.2.The expression of ZnT1 was increased in spinal cord following abdominal aorta occlusion and sub- sequent endotoxemia.It indicated that ZnT1 may play an important role in regulating the homeostasis of zinc in the early stage of spinal cord injury and may play an important role in the pathological physiological activities of spinal cord neurons. This result may provide new ideas for preventing the early stage＇s spinal cord injury.