CAJ | 학술논문

目的：探讨c-Jun氨基末端激酶（JNK）磷酸化14-3-3在大鼠缺血性脑损伤中的作用。方法20只大鼠均分为4组：假手术组、缺血复灌组、SP600125组和溶剂对照组。制作大鼠全脑缺血模型，应用免疫沉淀和免疫印迹法检测4组大鼠脑缺血复灌12 h海马CA1区神经元14-3-3磷酸化（p-14-3-3）、14-3-3与Bax结合、Bax在胞浆和线粒体的蛋白表达情况。结果与假手术组相比，缺血复灌组、溶剂对照组及SP600125组胞浆中的p-14-3-3蛋白、线粒体中的Bax蛋白均增高，14-3-3与Bax的结合降低，SP600125组的胞浆p-14-3-3蛋白、线粒体Bax蛋白低于缺血复灌组和溶剂对照组，14-3-3与Bax的结合高于缺血复灌组和溶剂对照组（均P<0.05）。结论 JNK磷酸化14-3-3在大鼠缺血性脑损伤中发挥了重要作用。
목적：탐토c-Jun안기말단격매（JNK）린산화14-3-3재대서결혈성뇌손상중적작용。방법20지대서균분위4조：가수술조、결혈복관조、SP600125조화용제대조조。제작대서전뇌결혈모형，응용면역침정화면역인적법검측4조대서뇌결혈복관12 h해마CA1구신경원14-3-3린산화（p-14-3-3）、14-3-3여Bax결합、Bax재포장화선립체적단백표체정황。결과여가수술조상비，결혈복관조、용제대조조급SP600125조포장중적p-14-3-3단백、선립체중적Bax단백균증고，14-3-3여Bax적결합강저，SP600125조적포장p-14-3-3단백、선립체Bax단백저우결혈복관조화용제대조조，14-3-3여Bax적결합고우결혈복관조화용제대조조（균P<0.05）。결론 JNK린산화14-3-3재대서결혈성뇌손상중발휘료중요작용。
Objective To investigate the effects of 14-3-3 phosphorylation (p-14-3-3) induced by C-Jun N-termi-nal kinase (JNK) on ischemic brain injury in rats. Methods Twenty rats were divided into 4 groups:sham operation group, ischemia-reperfusion group, SP600125 group and solvent control group. The rat model of cerebral ischemia was established. The p-14-3-3, the binding of 14-3-3 and Bax and the protein expression of Bax in cytoplasm and mitochondria in hippo-campal CA1 region were detected by immunoprecipitation (IP) and immunoblotting 12-hour after ischemia-reperfusion in four groups. Results Compared with the sham operation group, protein expression levels of p-14-3-3 in cytoplasm and Bax in mitochondria were significantly increased, the binding of 14-3-3 and Bax was significantly decreased in ischemia-re-perfusion group, solvent control group and SP600125 group. The protein expressions of p-14-3-3 and Bax were significantly lower in SP600125 group than those of ischemia-reperfusion group and solvent control group. The binding of 14-3-3 and Bax was significantly higher in SP600125 group than that of ischemia-reperfusion group and solvent control group (P <0.05). Conclusion 14-3-3 phosphorylation induced by JNK plays important effects on ischemic brain injury in rats.