CAJ | 학술논문

目的评价七氟醚麻醉对幼鼠海马c-Jun氨基末端激酶(JNK)表达和神经细胞凋亡的影响.方法健康雄性SD大鼠40只,日龄30～35 d,体重100～110 g,采用随机数字表法,将其随机分为2组(n=20):对照组(C组):吸入含有30%氧气的空氧混合气体5 h;七氟醚组(s组):吸入3%七氟醚5 h,并维持麻醉箱氧浓度为30%.苏醒后1 h时,每组随机处死10只大鼠,取两侧海马组织,分别采用免疫组化法和Western blot法测定磷酸化JNK(p-JNK)的表达水平,采用TUNEL法检测神经细胞凋亡情况.苏醒后24 h时,每组随机取10只大鼠,采用Morris水迷宫测试认知功能.结果与C组比较,S组海马组织p-JNK表达上调,凋亡细胞计数升高,潜伏期延长和平台象限停留时间缩短(P＜0.05或0.01).结论吸入3.0%七氟醚可能通过激活JNK信号通路,诱发海马神经细胞凋亡,从而导致幼鼠认知功能降低.
목적 평개칠불미마취대유서해마c-Jun안기말단격매(JNK)표체화신경세포조망적영향.방법 건강웅성SD대서40지,일령30～35 d,체중100～110 g,채용수궤수자표법,장기수궤분위2조(n=20):대조조(C조):흡입함유30%양기적공양혼합기체5 h;칠불미조(s조):흡입3%칠불미5 h,병유지마취상양농도위30%.소성후1 h시,매조수궤처사10지대서,취량측해마조직,분별채용면역조화법화Western blot법측정린산화JNK(p-JNK)적표체수평,채용TUNEL법검측신경세포조망정황.소성후24 h시,매조수궤취10지대서,채용Morris수미궁측시인지공능.결과 여C조비교,S조해마조직p-JNK표체상조,조망세포계수승고,잠복기연장화평태상한정류시간축단(P＜0.05혹0.01).결론 흡입3.0%칠불미가능통과격활JNK신호통로,유발해마신경세포조망,종이도치유서인지공능강저.
Objective To investigate the effects of sevoflurane anesthesia on the expression of c-Jun N-terminal kinase (JNK) and neuronal apoptosis in hippocampus in juvenile rats.Methods Forty healthy male SD rats, aged 30-35 days, weighing 100-110 g, were randomly divided into 2 groups (n = 20 each): control group (group C) and sevoflurane group (group S) . Group C inhaled a gas mixture of oxygen and air for 5 h and group S 3% sevoflurane for 5 h. The concentration of oxygen in both groups was maintained at 30% . Ten rats in each group were scarified at 1 h after regaining consciousness and the hippocampi removed for determination of phospho-JNK expression (by immuno-histochemistry and Western blot) and neuronal apoptosis (by TUNEL) . Another 10 rats were selected at 24 h after regaining consciousness to assess the cognitive function using Morris water maze. Results Compared with group C, phospho-JNK expression was significantly up-regulated, the number of apoptotic neurons increased, the latency prolonged and the duration of staying at the original platform quadrant shortened in group C ( P ＜ 0.05 or 0.01) . Conclusion Inhalation of 3.0% sevoflurane can induce neuronal apoptosis in hippocampus by activating JNK signaling pathway, thus leading to cognitive decline in juvenile rats.