实验性脊髓空洞前状态蛋白激酶C活性变化对NF-κB、IκB表达的影响

Effect of protein kinase C on expression of NF-κB and IκB in experimental presyrinx state

目的探讨蛋白激酶C（PKC）和核转录因子-κB（NF—κB）之间的关系及其在脊髓空洞前状态发病中的作用。方法用新西兰兔56只制作模型，术后1、3、7、14、21d用光镜观察上颈髓病理学演变；应用底物磷酸化法测定胞膜、胞浆PKC活性；应用免疫组化法测定NF—κB和IκB表达变化。结果高岭土组动物于术后第3d上颈髓轻度水肿，7—14d水肿达到高峰期，21d略有缓解；胞膜PKC活性术后1d出现增加（5．67±0．26pmol／mg／min），7—14d达到最高水平（13．27±3．15pmol／mg／min），21d开始回落（8．85±1．56pmol／mg／min），胞浆的PKC活性则呈相反趋势；NF—κB则于术后第1d明显升高（26．08％±2．36％），第7d达高峰（41．37％±3．22％），到两周时开始下降（37．56％±5．11％），IκB与NF-κB表达呈相反变化趋势。结论脊髓空洞前状态形成中出现PKC移位激活，可能通过激活NF—κB即PKC—NF—κB信号转导途径参与了脊髓空洞前状态的一系列病理过程。

Objective To investigate the relationship between protein Kinase C （PKC） and nuclear transcription factor-κB （NF-κB） and their roles in pathological development of experimental syringomyelia in rabbits. Methods The experimental syringomyelia models of rabbits were established by intra-cisternal injection of Kaolin. Pathological changes, PKC activity and the expression of NF-κB and IκB were measured with light microscopy, substrate phosphorylation and immunohistochemistry in 1 d, 3 d, 7 d, 14 d, and 21 d after operation respectively. Results Histological observation showed that the spinal cord edema in Kaolin group appeared at 1 st day after Kaolin injection, became more prominent at 3 rd day, reached its peak at 7 th day, and declined slowly after 3 weeks. Membrane PKC activity increased from 1 st day （5.67±0. 26 pmol/mg/min ）, reached its peak during 7 th to 14 th day （13.27±3.15 pmol/mg/min）, and then began to drop off （8.85±1.56 pmol/mg/min）. But cytoplasm PKC activity showed the opposite tendency to membrane PKC activity. NF-κB expression increased at 1 st day after operation （26. 08%±2. 36% ）, reached its peak at 7 th day （41.37%±3.22% ） and began to decline at 14 th day（37.56%±5.11% ）. Expression of IκB showed the opposite tendency to that of NF-κB at the same time points. Conclusion In presyrinx state of experimental syringomyelia, transloactional activation of PKC may vitalize NF-κB and involve in a series of pathological procedure by PKC-NF-κB signal pathway.