CAJ | 학술논문

目的探讨异丙酚对大鼠窒息性心脏停搏复苏后海马c-JUN氨基末端激酶(JNK)活化的影响.方法雄性SD大鼠40只,6月龄,体重350 ～ 380 g,采用随机数字表法,将其分为4组(n=10),假手术组(S组)仅动静脉置管和气管插管而不制备窒息性心脏停搏；窒息性心脏停搏复苏组(CA-CPR组)采用窒息法建立CA-CPR模型；异丙酚组(P组)于窒息前30 min静脉注射异丙酚20mg/kg,继之以40 mg·kg-1 ·h-1的速率静脉输注至复苏开始；生理盐水组(NS组)以等容量生理盐水替代异丙酚,余处理同P组.成功复苏后12 h时,处死大鼠,取脑组织,测定湿/干重(W/D)比；采用免疫组化法和Western blot法测定海马磷酸化JNK(p-JNK)的表达水平,并观察海马病理学结果.结果与S组比较,CA-CPR组、P组和NS组脑W/D比升高,海马p-JNK表达水平上调(P＜0.05或0.01)；与CA-CPR组比较,P组脑W/D比降低,海马p-JNK表达水平下调(P＜0.05或0.01),NS组上述指标差异无统计学意义(P＞0.05).P组海马病理学损伤较CA-CPR组减轻.结论异丙酚可抑制大鼠窒息性心脏停搏复苏后脑组织JNK的活化,从而减轻脑损伤.
목적 탐토이병분대대서질식성심장정박복소후해마c-JUN안기말단격매(JNK)활화적영향.방법 웅성SD대서40지,6월령,체중350 ～ 380 g,채용수궤수자표법,장기분위4조(n=10),가수술조(S조)부동정맥치관화기관삽관이불제비질식성심장정박；질식성심장정박복소조(CA-CPR조)채용질식법건립CA-CPR모형；이병분조(P조)우질식전30 min정맥주사이병분20mg/kg,계지이40 mg·kg-1 ·h-1적속솔정맥수주지복소개시；생리염수조(NS조)이등용량생리염수체대이병분,여처리동P조.성공복소후12 h시,처사대서,취뇌조직,측정습/간중(W/D)비；채용면역조화법화Western blot법측정해마린산화JNK(p-JNK)적표체수평,병관찰해마병이학결과.결과 여S조비교,CA-CPR조、P조화NS조뇌W/D비승고,해마p-JNK표체수평상조(P＜0.05혹0.01)；여CA-CPR조비교,P조뇌W/D비강저,해마p-JNK표체수평하조(P＜0.05혹0.01),NS조상술지표차이무통계학의의(P＞0.05).P조해마병이학손상교CA-CPR조감경.결론 이병분가억제대서질식성심장정박복소후뇌조직JNK적활화,종이감경뇌손상.
Objective To investigate the effect of propofol on the activation of c-Jun N-terminal kinase (JNK) in hippocampus following asphyxial cardiac arrest-resuscitation in rats.Methods Forty male Sprague-Dawley rats,aged 6 months,weighing 350-380 g,were randomly divided into 4 groups (n =l0 each):sham operation group (group S),asphyxial cardiac arrest-cardiopulmonary resuscitation group (group CA-CPR),propofol group (group P) and normal saline group (group NS).All the rats were tracheostomized and mechanically ventilated after anesthetization.Cardiac arrest was induced by clamping the tracheal tube at the end of exhalation until ECG activity disappeared and MAP ＜ 10 mm Hg.Resuscitation was started 3 min later.MAP ＞ 60 mm Hg and HR ＞ 250 bpm were considered to be signs of successful resuscitation.Propofol 2 mg/kg was injected intravenously at 30 min before asphyxia,followed by propofol infusion at a rate of 4 mg· kg-1 · h-1 until the start of resuscitation in group P,while the equal volume of normal saline was given in group NS.At 12 h after successful resuscitation,the animals were sacrificed and brains were harvested for determination of wet/dry brain weight (W/D) ratio in brain tissues and expression of phosphor-JNK (p-JNK) in hippocampus (by immuno-histochemistry and Western blot),and for examination of the pathological changes of hippocampus.Results Compared with group S,W/D ratio was significantly increased and the expression of p-JNK in hippocampus was up-regulated in CA-CPR,P and NS groups (P ＜ 0.05 or 0.01).Compared with group CA-CPR,W/D ratio was significantly decreased and the expression of p-JNK in hippocampus was down-regnlated in group P (P ＜ 0.05 or 0.01),and no significant change was found in the indexes mentioned above in group NS (P ＞ 0.05).The pathological changes of hippocampus were significantly attenuated in group P compared with group CA-CPR.Conclusion Propofol can inhibit the activation of JNK in hippocampus following asphyxial cardiac arrest-resuscitation in rats and thus reducing brain injury.