CAJ | 학술논문

目的探讨异丙酚对抑郁大鼠电休克处理后海马钙离子/钙调蛋白依赖性蛋白激酶Ⅱα(CaMKⅡα)活性的影响.方法健康成年雄性SPF级SD大鼠,体重180～220 g,2～3月龄,采用慢性轻度不可预见性应激法建立抑郁模型.取模型制备成功的大鼠40只,采用随机数字表法,将其随机分为4组(n=10):抑郁组(D组)腹腔注射生理盐水8 ml/kg；单纯异丙酚组(P组)腹腔注射异丙酚80mg/kg;单纯电休克组(E组)腹腔注射生理盐水8ml/kg后实施电休克处理；异丙酚联合电休克(DPE)组腹腔注射异丙酚80 mg/kg,待翻正反射消失后行电休克处理.以上处理每天1次,连续7d.于处理前1d和处理后1d采用糖水偏好实验评价抑郁状态.于处理前1d和处理后3d采用Morris水迷宫实验检测学习记忆能力.于Morris水迷宫实验完成后1d,采用免疫组织化学法检测大鼠海马磷酸化CaMKⅡα(pCaMKⅡα)及CaMKⅡα的表达,计算pCaMKⅡα/CaMKⅡα比.结果与D组比较,E组、DPE组糖水偏好比升高,E组逃避潜伏期延长,空间探索时间缩短,海马CaMKⅡα和pCaMKⅡα表达下调,pCaMKⅡα/CaMKⅡα比降低,DPE组逃避潜伏期缩短,空间探索时间延长,pCaMKⅡα表达上调(P＜0.05)；与E组比较,DPE组逃避潜伏期缩短,空间探索时间延长,CaMKⅡα和pCaMKⅡα表达上调,pCaMKⅡα/CaMKⅡα比升高(P＜0.05).结论异丙酚减轻抑郁大鼠电休克处理后认知功能损害的机制可能与增强海马CaMKⅡα的活性有关.
목적 탐토이병분대억욱대서전휴극처리후해마개리자/개조단백의뢰성단백격매Ⅱα(CaMKⅡα)활성적영향.방법 건강성년웅성SPF급SD대서,체중180～220 g,2～3월령,채용만성경도불가예견성응격법건립억욱모형.취모형제비성공적대서40지,채용수궤수자표법,장기수궤분위4조(n=10):억욱조(D조)복강주사생리염수8 ml/kg；단순이병분조(P조)복강주사이병분80mg/kg;단순전휴극조(E조)복강주사생리염수8ml/kg후실시전휴극처리；이병분연합전휴극(DPE)조복강주사이병분80 mg/kg,대번정반사소실후행전휴극처리.이상처리매천1차,련속7d.우처리전1d화처리후1d채용당수편호실험평개억욱상태.우처리전1d화처리후3d채용Morris수미궁실험검측학습기억능력.우Morris수미궁실험완성후1d,채용면역조직화학법검측대서해마린산화CaMKⅡα(pCaMKⅡα)급CaMKⅡα적표체,계산pCaMKⅡα/CaMKⅡα비.결과 여D조비교,E조、DPE조당수편호비승고,E조도피잠복기연장,공간탐색시간축단,해마CaMKⅡα화pCaMKⅡα표체하조,pCaMKⅡα/CaMKⅡα비강저,DPE조도피잠복기축단,공간탐색시간연장,pCaMKⅡα표체상조(P＜0.05)；여E조비교,DPE조도피잠복기축단,공간탐색시간연장,CaMKⅡα화pCaMKⅡα표체상조,pCaMKⅡα/CaMKⅡα비승고(P＜0.05).결론 이병분감경억욱대서전휴극처리후인지공능손해적궤제가능여증강해마CaMKⅡα적활성유관.
Objective To investigate the effects of propofol on calcium/calmodulin-dependent protein kinase Ⅱ α ( CaMK Ⅱ α) activity in hippocampus in mentally depressed rats after electroconvulsive therapy (ECT).Methods Healthy adult male SD rats aged 2-3 months weighing 180-220 g were used in this study.Mentally depressed model was induced by chronic unpredictable mild stress.Forty mentally depressed rats were randomly divided into 4 groups (n =10 each): mental depression group (group D),propofol group (group P),ECT group (group E),propofol + ECT group (group DPE).Groups D and P received intraperitoneal normal saline 8 ml/kg or propofol 80 mg/kg once a day for 7 consecutive days respectively.Group E received ECT once a day for 7 consecutive days.Group DPE received propofol 80 mg/kg + ECT once a day for 7 consecutive days.Sucrose preference test was performed at 1 d before and 1 d after treatment,and Morris water maze test was performed at 1 d before and 3 d after treatment.The rats were sacrificed after Morris water maze test,and hippocampi were removed for determination of CaMK Ⅱ α and phosphorylated CaMK Ⅱ α(pCaMK Ⅱ α )expression,and pCaMK Ⅱ α/CaMK Ⅱ α ratio was caculated.Results Compared with group D,the sucrose preference percentage was significantly increased in groups E and DPE,the escape latency prolonged and space exploration time shortened,and the expression of CaMK Ⅱ α and pCaMK Ⅱ α down-regulated,pCaMK Ⅱ α/CaMK Ⅱ α ratio decreased in group E,the escape latency was significantly shortened and space exploration time prolonged,and the expression of pCaMK Ⅱ α up-regulated in group DPE ( P ＜ 0.05).Compared with group E,the escape latency was significantly shortened,space exploration time prolonged,and the expression of CaMK Ⅱ α and pCaMK Ⅱ α up-regulated,and pCaMK Ⅱ α/CaMK Ⅱ α ratio increased in group DPE ( P ＜ 0.05).Conclusion Propofol can reduce the cognition impairment induced by ECT in mentally depressed rats through enhancing CaMK Ⅱ α activity in hippocampus.