CAJ | 학술논문

目的评价c-Jun氨基端激酶(JNK)信号通路在大鼠窒息性心跳骤停复苏后脑损伤中的作用.方法健康雄性SD大鼠40只,体重300～ 350 g,采用随机数字表法,将其随机分为4组(n=10):假手术组(SH组)、心跳骤停组(CA组)、JNK抑制剂SP600125组(SP组)和二甲基亚砜组(DMSO组).静脉注射维库溴铵2mg/kg后行机械通气,维持PET CO2 35～ 45 mm Hg.CA组、SP组和DMSO组机械通气稳定5 min后注射维库溴铵1 mg/kg,1 min后停止机械通气,于呼气末时夹闭气管导管,制备窒息性心跳骤停模型.心跳骤停3 min后,开放气管导管行机械通气,立即进行复苏.SP组静脉注射SP600125 20mg/kg,DMSO组静脉注射DMSO 0.2 ml.于心跳恢复后5h时处死大鼠,取脑组织,测定湿/干重比(W/D比)和细胞凋亡情况,观察病理学结果.结果与SH组比较,CA组、SP组和DMSO组脑组织W/D比和凋亡细胞计数升高(P＜0.05)；与CA组和DMSO组比较,SP组脑组织W/D比和凋亡细胞计数下降(P＜0.05),病理学损伤减轻；CA组和DMSO组脑组织W/D比和凋亡细胞计数比较差异无统计学意义(P＞0.05).结论 JNK信号通路参与了大鼠窒息性心跳骤停复苏诱发脑损伤的病理生理过程.
목적 평개c-Jun안기단격매(JNK)신호통로재대서질식성심도취정복소후뇌손상중적작용.방법 건강웅성SD대서40지,체중300～ 350 g,채용수궤수자표법,장기수궤분위4조(n=10):가수술조(SH조)、심도취정조(CA조)、JNK억제제SP600125조(SP조)화이갑기아풍조(DMSO조).정맥주사유고추안2mg/kg후행궤계통기,유지PET CO2 35～ 45 mm Hg.CA조、SP조화DMSO조궤계통기은정5 min후주사유고추안1 mg/kg,1 min후정지궤계통기,우호기말시협폐기관도관,제비질식성심도취정모형.심도취정3 min후,개방기관도관행궤계통기,립즉진행복소.SP조정맥주사SP600125 20mg/kg,DMSO조정맥주사DMSO 0.2 ml.우심도회복후5h시처사대서,취뇌조직,측정습/간중비(W/D비)화세포조망정황,관찰병이학결과.결과 여SH조비교,CA조、SP조화DMSO조뇌조직W/D비화조망세포계수승고(P＜0.05)；여CA조화DMSO조비교,SP조뇌조직W/D비화조망세포계수하강(P＜0.05),병이학손상감경；CA조화DMSO조뇌조직W/D비화조망세포계수비교차이무통계학의의(P＞0.05).결론 JNK신호통로삼여료대서질식성심도취정복소유발뇌손상적병리생리과정.
Objective To evaluate the role of JNK signal pathway in brain injury after resuscitation in a rat model of asphyxia cardiac arrest.Methods Forty healthy male SD rats 'weighing 300-350 g were randomly divided into 4 groups ( n =10 each):sham operation group (group SH) ; cardiac arrest group (group CA) ; group SP600125-JNK inhibitor (group SP) and dimethyl sulfexide (DMSO) group.The rats were anesthetized with intraperitoneal pentobarbital 45 mg/kg,tracheostomized and mechanically ventilated.PETCO2 was maintained at 35-45 mm Hg.Femoral artery and vein were cannulated for BP monitoring and fluid infusion.Cardiac arrest was induced by clamping tracheal tube until ECG activity disappeared and MAP ＜ 10 mm Hg.Resuscitation was started at 3 min after cardiac arrest.MAP ＞ 60 mm Hg and HR ＞ 250 bpm were considered to be signs of successful resuscitation.SP600125 20 mg/kg and DMSO 0.2 ml were injected iv as soon as chest compression was started in groups SP and DMSO respectively.The animals were sacrificed at 5 h after successful resuscitation and their brains were removed for determination of wet/dry (W/D) weight ratio and microscopic examination of hippocampus.Neuronal apoptosis was detected by TUNEL.Results Cardiac arrest significantly increased W/D ratio and the number of apoptotic cells in group CA.SP600125 iv significantly attenuated the cardiac arrest-induced increase in W/D ratio and the number of apoptotic cells but DMSO did not.Conclusion JNK signal pathway is involved in the brain injury after resuscitation in a rat model of asphyxia cardiac arrest.