CAJ | 학술논문

目的评价线粒体介导海马神经元凋亡在七氟醚麻醉致老龄大鼠认知功能障碍中的作用.方法健康雄性SD大鼠60只,20月龄,体重550 ～ 600 g,采用随机数字表法,将其分为2组(n=30):对照组(C组)和七氟醚麻醉组(S组),分别吸入氧气和3％七氟醚4h.麻醉后1d取10只大鼠,采用Morris水迷宫实验评价认知功能,连续6d.分别于麻醉后1、6d时取10只大鼠,取海马组织,采用流式细胞术测定海马神经元凋亡率和线粒体膜电位(MMP),采用Western blot法测定海马神经元活化caspase-3和胞浆细胞色素c的表达.结果与C组比较,S组逃避潜伏期延长,穿越平台次数、平台所在象限停留时间百分比和海马神经元MMP降低,海马神经元凋亡率增加,海马神经元活化caspase-3表达和胞浆细胞色素c表达上调(P＜0.05).结论七氟醚麻醉导致老龄大鼠认知功能障碍的机制与激活线粒体介导海马神经元凋亡有关.
목적 평개선립체개도해마신경원조망재칠불미마취치노령대서인지공능장애중적작용.방법 건강웅성SD대서60지,20월령,체중550 ～ 600 g,채용수궤수자표법,장기분위2조(n=30):대조조(C조)화칠불미마취조(S조),분별흡입양기화3％칠불미4h.마취후1d취10지대서,채용Morris수미궁실험평개인지공능,련속6d.분별우마취후1、6d시취10지대서,취해마조직,채용류식세포술측정해마신경원조망솔화선립체막전위(MMP),채용Western blot법측정해마신경원활화caspase-3화포장세포색소c적표체.결과 여C조비교,S조도피잠복기연장,천월평태차수、평태소재상한정류시간백분비화해마신경원MMP강저,해마신경원조망솔증가,해마신경원활화caspase-3표체화포장세포색소c표체상조(P＜0.05).결론 칠불미마취도치노령대서인지공능장애적궤제여격활선립체개도해마신경원조망유관.
Objective To evaluate the role of mitochondria-mediated apoptosis in hippocampal neurons in sevoflurane anesthesia-induced cognitive dysfunction in aged rats.Methods Sixty healthy male Sprague-Dawley rats,aged 20 months,weighing 550-600 g,were randomly divided into 2 groups (n =30 each) using a random number table:control group (group C) and sevoflurane anesthesia group (group S).Animals inhaled pure oxygen and 3 ％ sevoflurane for 4 h in C and S groups,respectively.Ten rats were chosen at 1 and 6 days after anesthesia and hippocampal tissues were obtained for detection of cell apoptosis and mitochondrial membrane potential (MMP) (using flow cytometry) and expression of cytochrome c (Cyt c) in cytoplasm and activated caspase-3 in hippocampal neurons (by Western blot).The apoptotic rate was calculated.Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform,the percentage of time of staying at the original platform quadrant and MMP were decreased,the apoptotic rate was increased,and the expression of activated caspase-3 and Cyt c in cytoplasm was up-regulated in.group S.Conclusion The mechanism by which sevoflurane anesthesia induces cognitive dysfunction is related to the activation of mitochondria-mediated apoptosis in hippocampal neurons of aged rats.