CAJ | 학술논문

目的探讨异丙酚对氯胺酮诱发新生大鼠脑损伤的影响.方法新生SD大鼠80只,日龄7 d,雌雄不拘,体重12～20 g,采用随机数字表法,将大鼠随机分为4组(n=20):生理盐水对照组(NS组)腹腔注射生理盐水1 ml;氯胺酮致脑损伤组(K组)、异丙酚对照组(P组)和异丙酚+氯胺酮组(PK组)分别腹腔注射氯胺酮70mg/kg、异丙酚70mg/kg、异丙酚70mg/kg+氯胺酮70mg/kg,每隔2 h注射1次,共3次.于苏醒后24 h时各组随机取10只大鼠,处死后取海马组织,采用TUNEL法检测海马CA1区神经元凋亡情况,计算凋亡率,采用免疫组化法检测Bcl-2和Bax的蛋白表达,腹腔注射后21d时各组余大鼠采用Morris水迷宫实验测定学习记忆功能(逃避潜伏期和穿越平台次数).结果与NS组相比,K组神经元凋亡率升高,P组和PK组Bcl-2蛋白表达上调,其余各组Bax蛋白表达上调,逃避潜伏期延长,穿越平台次数减少(P＜0.05或0.01);与K组相比,PK组神经元凋亡率降低,P组Bax蛋白表达下调,P组和PK组Bcl-2蛋白表达上调,逃避潜伏期缩短,穿越平台次数增加(P＜0.05).结论异丙酚可减轻氯胺酮诱发新生大鼠的脑损伤,可能与其调节Bcl-2和Bax蛋白表达从而抑制海马神经元凋亡有关.
목적 탐토이병분대록알동유발신생대서뇌손상적영향.방법 신생SD대서80지,일령7 d,자웅불구,체중12～20 g,채용수궤수자표법,장대서수궤분위4조(n=20):생리염수대조조(NS조)복강주사생리염수1 ml;록알동치뇌손상조(K조)、이병분대조조(P조)화이병분+록알동조(PK조)분별복강주사록알동70mg/kg、이병분70mg/kg、이병분70mg/kg+록알동70mg/kg,매격2 h주사1차,공3차.우소성후24 h시각조수궤취10지대서,처사후취해마조직,채용TUNEL법검측해마CA1구신경원조망정황,계산조망솔,채용면역조화법검측Bcl-2화Bax적단백표체,복강주사후21d시각조여대서채용Morris수미궁실험측정학습기억공능(도피잠복기화천월평태차수).결과 여NS조상비,K조신경원조망솔승고,P조화PK조Bcl-2단백표체상조,기여각조Bax단백표체상조,도피잠복기연장,천월평태차수감소(P＜0.05혹0.01);여K조상비,PK조신경원조망솔강저,P조Bax단백표체하조,P조화PK조Bcl-2단백표체상조,도피잠복기축단,천월평태차수증가(P＜0.05).결론 이병분가감경록알동유발신생대서적뇌손상,가능여기조절Bcl-2화Bax단백표체종이억제해마신경원조망유관.
Objective To investigate the effect of propofol on the cerebral injury induced by ketamine in neonatal rats. Methods Eighty 7-day-old SD rats of both sexes, weighing 12-20 g, were randomly divided into 4 groups (n = 20 each): normal saline (NS) group, ketamine-induced cerebral injury group (group K), propofol group (group P) and propofol combined with ketamine group (group PK). Group NS received intraperitoneal NS 1 ml. In groups K, P and PK, ketamine 70 mg/kg, propofol 70 mg/kg and propofol 70 mg/kg + ketamine 70 mg/kg were injected intraperitoneally once every 2 h for 3 times respectively. Ten rats in each group were selected and sacrificed at 24 h after emergence from anesthesia and the hippocampi obtained to determine the neuronal apoptosis (by TUNEL) and Bcl-2 and Bax protein expression(by immunohitochemistry). The apoptosis rate was calculated.The other 10 rats in each group were selected at 21 days after the intraperitoneal injection and the learning and memory functions (escape latency and frequency of crossing the original platform) were evaluated using Morris water maze. Results Compared with group NS, the apoptosis rate was significantly increased in group K, Bcl-2 protein expression was up-regulated in groups P and PK, and Bax protein expression was up-regulated, the escape latency was significantly prolonged and the frequency of crossing the original platform was significantly decreased in the other groups (P ＜ 0.05 .or 0.01 ). Compared with group K, the apoptosis rate was significantly decreased in group PK, Bax protein expression was down-regulated in group P, and Bcl-2 protein expression was up-regulated,the escape latency was significantly shortened and the frequency of crossing the original platform was significantlyincreased in groups P and PK ( P ＜ 0.05). Conclusion Propofol can reduce the cerebral injury induced by ketamine in neonatal rats, and the regulation of the Bcl-2 and Bax protein expression and inhibition of the neuronal apoptosis in hippocampus may be involved in the mechanism.