CAJ | 학술논문

目的探讨大鼠内毒素性急性肺损伤(acute lung injury,ALI)时应用丙泊酚后处理对肺组织磷酸化c-Jun氨基末端激酶(phospho-c-Jun terninal kinnase,p-JNK)的影响.方法 96只雄性SD大鼠按数字随机表法分为4组(每组24只):生理盐水对照组(A组)；内毒素[有效成分为脂多糖(lipopolysaccharides,LPS)]致伤组5 mg/kg尾静脉注射,B组)；丙泊酚低剂量治疗组(丙泊酚2 mg/kg诱导后,4 mg· kg-1·h-1维持,C组)；丙泊酚高剂量治疗组(丙泊酚4 mg/kg诱导后,8 mg· kg-1·h-1维持,D组).每组大鼠均在诱导后1、2、3、4 h时经放血处死大鼠(采用放血法随机活杀6只大鼠并留取肺组织标本),用免疫蛋白印迹法(western-blot)和免疫组织化学法(immunocytoche-mical,IHC)检测肺组织c-Jun氨基末端激酶(c-Jun terninal kinase,JNK)磷酸化的水平.结果 western-blot和IHC显示B、C、D3组各时点肺组织JNK磷酸化水平较A组均显著升高(P=0.02～0.03＜0.05或P=0.006～0.008＜0.01),3h时western-blot达到了322±32,比A组相同时点有显著升高(P=0.002＜0.01)；IHC显示p-JNK为21.7±4.4,比A组也有明显的增多(P=0.003＜0.01).C组和D组大鼠的肺组织p-JNK与B组各时点相比有显著的降低(P=0.03 ～0.04＜0.05或P=0.007～0.008＜0.01),western-blot显示3 h p-JNK时分别下降到了235±26和179±21,而IHC则降低至15.1±3.1和12.3±1.7.D组p-JNK与C组相比,在诱导后3h也有显著地下降,其余各时点相比无统计学意义.结论丙泊酚可以显著抑制内毒索性ALI大鼠肺组织中p-JNK的表达.
목적 탐토대서내독소성급성폐손상(acute lung injury,ALI)시응용병박분후처리대폐조직린산화c-Jun안기말단격매(phospho-c-Jun terninal kinnase,p-JNK)적영향.방법 96지웅성SD대서안수자수궤표법분위4조(매조24지):생리염수대조조(A조)；내독소[유효성분위지다당(lipopolysaccharides,LPS)]치상조5 mg/kg미정맥주사,B조)；병박분저제량치료조(병박분2 mg/kg유도후,4 mg· kg-1·h-1유지,C조)；병박분고제량치료조(병박분4 mg/kg유도후,8 mg· kg-1·h-1유지,D조).매조대서균재유도후1、2、3、4 h시경방혈처사대서(채용방혈법수궤활살6지대서병류취폐조직표본),용면역단백인적법(western-blot)화면역조직화학법(immunocytoche-mical,IHC)검측폐조직c-Jun안기말단격매(c-Jun terninal kinase,JNK)린산화적수평.결과 western-blot화IHC현시B、C、D3조각시점폐조직JNK린산화수평교A조균현저승고(P=0.02～0.03＜0.05혹P=0.006～0.008＜0.01),3h시western-blot체도료322±32,비A조상동시점유현저승고(P=0.002＜0.01)；IHC현시p-JNK위21.7±4.4,비A조야유명현적증다(P=0.003＜0.01).C조화D조대서적폐조직p-JNK여B조각시점상비유현저적강저(P=0.03 ～0.04＜0.05혹P=0.007～0.008＜0.01),western-blot현시3 h p-JNK시분별하강도료235±26화179±21,이IHC칙강저지15.1±3.1화12.3±1.7.D조p-JNK여C조상비,재유도후3h야유현저지하강,기여각시점상비무통계학의의.결론 병박분가이현저억제내독색성ALI대서폐조직중p-JNK적표체.
Objective To investigate the effects of c-Jun terninal kinase(JNK)activation post-trested by propofol on lipopolysaccharide-induced acute lung injury.Methods Ninety six male SD rats were randomly divided into 4 equal groups(n=24):the control group(0.9％ sodium chloride group); Lipopolysaccharides(LPS)group(intravenous injection of LPS 5 mg/kg); low dose of propofol group(2 mg/kg induced and 4 mg·kg1·h-1 maintained); large dose of propofol group(4 mg/kg induced and 8 mg·kg-1 ·h-1 maintained).Six rats were killed at each time point after LPS intravenous administration(saline in group A)and the lungs were harved and the activation of Phospho c-Jun terninal kinase(p-JNK)was recorded in the lung tissues by the method of western-blot and Immunocytoche-mical(IHC).Results Western-blot and IHC shown that the activation of JNK in the lung tissues increased significantly after LPS administration(P=0.02-0.03＜0.05 or P=0.006-0.008＜0.01).The number ofp-JNK was 322±32 and 21.7±4.4 shown by western-blot and IHC at the time point of 3 h after LPS administration.The p-JNK at all time points declined significantly after treatment with propofol in group C and group D and the p-JNK declined to 235±26 and 179±21(western-blot)and 15.1±3.1 and 12.3±1.7(IHC)at the time point of 3 h.Compared with group C,p-JNK declined more than those in group D at the time point of 3 h after after LPS administration.Conclusion Treatment with propofol can significantly attenuate the p-JNK expression in LPS-induced acute lung injury in rats.