中华行为医学与脑科学杂志
中華行為醫學與腦科學雜誌
중화행위의학여뇌과학잡지
CHINESE JOURNAL OF BEHAVIORAL MEDICINE AND BRAIN SCIENCE
2015年
5期
397-401
,共5页
杨坤%于雪%王敬兰%胡义秋
楊坤%于雪%王敬蘭%鬍義鞦
양곤%우설%왕경란%호의추
度洛西汀%抑郁%S100B%ERK1/2-NF-κB
度洛西汀%抑鬱%S100B%ERK1/2-NF-κB
도락서정%억욱%S100B%ERK1/2-NF-κB
Duloxetine%Depression%S100B%ERK1/2-NF-κB
目的 探讨度洛西汀对抑郁模型大鼠行为及海马S100B和信号通路ERK1/2-NF-κB表达的影响.方法 选取慢性轻度不可预知应激刺激法制备50只抑郁症模型大鼠,将其随机分为非干预组(B组,n=10)、不同用药时间的度洛西汀干预组C、D、E和F组,每组各10只.10只健康大鼠为对照组(A组).各组灌胃:A组和B组(生理盐水28 d),C组(生理盐水27d+度洛西汀1 d)、D组(生理盐水21d+度洛西汀7d)、E组(生理盐水14d+度洛西汀14 d)和F组(度洛西汀28 d)].灌胃结束,应用旷场试验、糖水偏爱试验检测大鼠行为改变;Western blot检测各组海马S100B、ERK1/2及NF-κB的表达.结果 E和F组大鼠干预28 d后旷场试验水平得分、垂直运动得分与潜伏期分别为(69.68±14.61)分和(70.66±11.53)分,(20.94±10.92)分和(20.32±8.85)分,(1.1±0.4)s和(1.0±0.4)s,与A组(71.19±12.08)分、(20.42±8.76)分、(1.0±0.3)s比较,均差异无统计学意义(P＞0.05);E、F组与其他两组比较,水平运动得分和垂直运动得分升高,潜伏期降低.最后一次应激结束后所进行的糖水偏爱实验显示A组糖水消耗率显著高于其他组,表明抑郁模型建立成功.灌胃28 d后B组糖水消耗率[(43±15)％]显著较A、E、F组[(63±11)％,(65±21)％,(67±6)％]减少(P＜0.05).A、E、F组大鼠海马S100B、pERK1/2及pNF-κB表达显著高于B组(P＜0.05).结论 度洛西汀能够改善抑郁模型大鼠的行为能力,2周以上起效,其机制可能通过S100B激活海马的信号通路ERK1/2-NF-κB发挥作用.
目的 探討度洛西汀對抑鬱模型大鼠行為及海馬S100B和信號通路ERK1/2-NF-κB錶達的影響.方法 選取慢性輕度不可預知應激刺激法製備50隻抑鬱癥模型大鼠,將其隨機分為非榦預組(B組,n=10)、不同用藥時間的度洛西汀榦預組C、D、E和F組,每組各10隻.10隻健康大鼠為對照組(A組).各組灌胃:A組和B組(生理鹽水28 d),C組(生理鹽水27d+度洛西汀1 d)、D組(生理鹽水21d+度洛西汀7d)、E組(生理鹽水14d+度洛西汀14 d)和F組(度洛西汀28 d)].灌胃結束,應用曠場試驗、糖水偏愛試驗檢測大鼠行為改變;Western blot檢測各組海馬S100B、ERK1/2及NF-κB的錶達.結果 E和F組大鼠榦預28 d後曠場試驗水平得分、垂直運動得分與潛伏期分彆為(69.68±14.61)分和(70.66±11.53)分,(20.94±10.92)分和(20.32±8.85)分,(1.1±0.4)s和(1.0±0.4)s,與A組(71.19±12.08)分、(20.42±8.76)分、(1.0±0.3)s比較,均差異無統計學意義(P＞0.05);E、F組與其他兩組比較,水平運動得分和垂直運動得分升高,潛伏期降低.最後一次應激結束後所進行的糖水偏愛實驗顯示A組糖水消耗率顯著高于其他組,錶明抑鬱模型建立成功.灌胃28 d後B組糖水消耗率[(43±15)％]顯著較A、E、F組[(63±11)％,(65±21)％,(67±6)％]減少(P＜0.05).A、E、F組大鼠海馬S100B、pERK1/2及pNF-κB錶達顯著高于B組(P＜0.05).結論 度洛西汀能夠改善抑鬱模型大鼠的行為能力,2週以上起效,其機製可能通過S100B激活海馬的信號通路ERK1/2-NF-κB髮揮作用.
목적 탐토도락서정대억욱모형대서행위급해마S100B화신호통로ERK1/2-NF-κB표체적영향.방법 선취만성경도불가예지응격자격법제비50지억욱증모형대서,장기수궤분위비간예조(B조,n=10)、불동용약시간적도락서정간예조C、D、E화F조,매조각10지.10지건강대서위대조조(A조).각조관위:A조화B조(생리염수28 d),C조(생리염수27d+도락서정1 d)、D조(생리염수21d+도락서정7d)、E조(생리염수14d+도락서정14 d)화F조(도락서정28 d)].관위결속,응용광장시험、당수편애시험검측대서행위개변;Western blot검측각조해마S100B、ERK1/2급NF-κB적표체.결과 E화F조대서간예28 d후광장시험수평득분、수직운동득분여잠복기분별위(69.68±14.61)분화(70.66±11.53)분,(20.94±10.92)분화(20.32±8.85)분,(1.1±0.4)s화(1.0±0.4)s,여A조(71.19±12.08)분、(20.42±8.76)분、(1.0±0.3)s비교,균차이무통계학의의(P＞0.05);E、F조여기타량조비교,수평운동득분화수직운동득분승고,잠복기강저.최후일차응격결속후소진행적당수편애실험현시A조당수소모솔현저고우기타조,표명억욱모형건립성공.관위28 d후B조당수소모솔[(43±15)％]현저교A、E、F조[(63±11)％,(65±21)％,(67±6)％]감소(P＜0.05).A、E、F조대서해마S100B、pERK1/2급pNF-κB표체현저고우B조(P＜0.05).결론 도락서정능구개선억욱모형대서적행위능력,2주이상기효,기궤제가능통과S100B격활해마적신호통로ERK1/2-NF-κB발휘작용.
Objective To analyze the effect of duloxetine on S100B and signal pathway ERK1/2-NF-κB expression in hippocampus in depression rat.Methods Chronic unpredictable mild stimulation was used to establish depressive model rats (n=50).They were randomly divided into no-intervention group (n=10),different treatment time of duloxetine group (C,D,E,F group,10 rats in each group)and then 10 normal rats were selected as control group.Behavior tests including open-field test and the saccharine preference test were used to test the behavioral change of rats after 28 days intragastric administration.Western blot was used to detect S100B,t-ERK1/2,pERK 1/2,t-NF-κB and pNF-κB expression in hippocampus.Results In open-field test,the crossing score,rearing score and latency of the rats in E,F group were (69.68± 14.61) and (70.66± 11.53) score,(20.94 ± 10.92) and (20.32±8.85) score,(1.1±0.4)s and(1.0±0.4) s respectively,and showed no significant difference with those of control group ((71.19±12.08) score,(20.42±8.76) score,(1.0±0.3)s) after 28 d intragastric administration (P＞0.05),while the level score,vertical score were significantly higher than those in depressive model (P＜ 0.05).In the saccharine preference test,the rats in E,F and control group exhibited increased saccharin preference compared with depressive model rats (P＜0.05).The rats in E,F and control group exhibited increased S100B,pERK1/2 and pNF-κB expression in hippocampus compared with depressive model rats (P＜0.05).Conclusion Duloxetine improves the behavioral ability of depression rat and exerts effect after 2 weeks.The ERK1/2-NF-κB signal pathway in hippocampus may participate in this mechanism.
