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目的探讨PKC在脊髓空洞前状态中活性变化及其对AQP4调控作用。方法用新西兰兔56只制作模型,术后1、3、7、14、21d用免疫组织化学技术检测AQP4表达变化、应用底物磷酸化法测定胞膜、胞浆PKC活性。结果 Kaolin组动物AQP4于术后3 d开始减弱(IA 320.5± 44.2),7-14 d达到最低水平(IA 258.7±26.5),到21 d时有所回升(IA 321.5±46.1);胞膜PKC 活性术后1 d出现增加每分钟(5.67±0.26)pmol/mg,7-14 d达到最高水平每分钟(13.27±3.15 pmol/mg),21 d开始回落每分钟(8.85±1.56)pmol/mg,胞浆的PKC活性则呈相反趋势。结论脊髓空洞前状态形成中出现PKC移位激活,对AQP4进行磷酸化,参与了缺血、缺氧性脊髓水肿的形成。
Objective To investigate the changes of PKC activity in the pre-syringomyelia and its role in the regulation of AQP4. Methods Fifty-six New Zealand rabbits were used to make the model. The expression of AQP4 was detected by immunohistochemistry on day 1, 3, 7, 14 and 21 after operation. The phospholipid activity of PKC was assayed by substrate phosphorylation assay. Results The AQP4 in Kaolin group began to decrease at 3 days after operation (IA 320.5 ± 44.2), reached the lowest level at 7-14 days (IA 258.7 ± 26.5), and then recovered at 21 days (IA 321.5 ± 46.1). The cell membrane PKC activity increased by 5.67 ± 0.26 pmol / mg on the 1st postoperative day and reached the highest level on the 7-14 day postoperatively (13.27 ± 3.15 pmol / Mg), 21d began to fall down (8.85 ± 1.56) pmol / mg, cytoplasmic PKC activity showed the opposite trend. Conclusions PKC shift activation occurs in the presymptomatic state of syringomyelia and phosphorylates AQP4, which is involved in the formation of ischemic and hypoxic spinal cord edema.