脊髓缺血损伤合并脓毒症后脊髓神经生长因子酪氨酸激酶A表达的研究

The expression of nerve growth factor, tyrosine kinase A in spinal cord in rats with spinal cord ischemia injury and subsequent endotoxemia

目的 研究腹主动脉阻断后合并内毒素攻击时大鼠脊髓的病理改变及脊髓组织中神经生长因子（nerve growth factor,NGF）、酪氨酸激酶A（tyrosine kinase A,Trk A）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NGF、TrkA的表达规律.结果 ①病理结果改变：除S组外,I/R组、LPS组、VR＋ LPS组3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：S组＜I/R组＜LPS组＜I/R＋ LPS组;②免疫组化结果：脊髓损伤组NGF的表达较S组均增加,脊髓损伤组Trk A的表达较S组均减少（P＜0.05）.结论 ①腹主动脉阻断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NGF表达上调,Trk A表达下调,NGF表达上调可能对机体内源性炎症调控过度具有重要意义,Trk A在早期脊髓损伤中的意义还有待于更深入的研究.

Objective To investigate the pathology change and the expression of nerve growth factor （NGF） and tyrosine kinase A （Trk A） of rat spinal cord following abdominal aorta occlusion 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）.Hematoxylin and eosin staining was used to examine the pathology change in the spinal cord,and immunohistochemistry （IHC） was used to measure the expression of NGF and Trk A.Results ①The pathology change：all groups except for S group showed obvious spinal cord injuries.The rank of spinal cord injures was S group ＜ I/R group ＜ LPS group ＜ I/R ＋ LPS group.②Immunohistochemistry：the expression of NGF in spinal cord injury groups were higher than that in sham group; the expression of Trk A in spinal cord injury groups were lower than that in sham group.Conclusion ①Abdominal aorta occlusion and subsequent endotoxemia can cause serious spinal cord injury.②The expression of NGF is increased and Trk A is decreased in spinal cord following abdominal aorta occlusion and subsequent endotoxemia.It suggests that NGF may play an important role in regulating inflammatory response.The role of Trk A in the early stage of spinal cord injury needs to be studied.