CAJ | 학술논문

目的探讨脓毒症时心肌损害的原因及p38丝裂原激活蛋白激酶(MAPK)抑制剂的保护作用.方法健康清洁级雄性SD大鼠66只,采用随机数字表法分为空白组6只,对照组30只,治疗组30只.空白组仅行麻醉,对照组和治疗组采用盲肠结扎并穿刺术制作脓毒症模型,在不同时间点观察大鼠心肌酶(CK-MB)、血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)的浓度及其mRNA在心肌的表达.结果术后血清TNF-α、IL-1β进行性升高,CK-MB也显著升高.正常心肌组织微量表达IL-1β mRNA,不表达TNF-αmRNA,脓毒症时两者大量表达.血清TNF-α、IL-1β浓度及其mRNA在心肌中的表达与心肌损害程度呈显著正相关(相关系数分别为0.918、0.795、0.905、0.768).应用p38MAPK抑制剂SB203580后,血清TNF-α、IL-1浓度显著降低,其mRNA在心肌中的表达减少,同时血CK-MB减低.结论 TNF-α、IL-1的大量释放及其在心肌中的表达是脓毒症心肌损害的原因之一,通过调控p38MAPK信号通路可对脓毒症鼠心肌损害起保护作用.
목적 탐토농독증시심기손해적원인급p38사렬원격활단백격매(MAPK)억제제적보호작용.방법 건강청길급웅성SD대서66지,채용수궤수자표법분위공백조6지,대조조30지,치료조30지.공백조부행마취,대조조화치료조채용맹장결찰병천자술제작농독증모형,재불동시간점관찰대서심기매(CK-MB)、혈청종류배사인자-α(TNF-α)、백세포개소-1β(IL-1β)적농도급기mRNA재심기적표체.결과 술후혈청TNF-α、IL-1β진행성승고,CK-MB야현저승고.정상심기조직미량표체IL-1β mRNA,불표체TNF-αmRNA,농독증시량자대량표체.혈청TNF-α、IL-1β농도급기mRNA재심기중적표체여심기손해정도정현저정상관(상관계수분별위0.918、0.795、0.905、0.768).응용p38MAPK억제제SB203580후,혈청TNF-α、IL-1농도현저강저,기mRNA재심기중적표체감소,동시혈CK-MB감저.결론 TNF-α、IL-1적대량석방급기재심기중적표체시농독증심기손해적원인지일,통과조공p38MAPK신호통로가대농독증서심기손해기보호작용.
Objective To investigate the protection function of p38MAPK inhibitor against myocardial inju-ry in sepsis. Methods The cecal ligation and puncture was adopted to build up sepsis model. The levels of serum CK-MB,TNF-alpha and IL-lbeta at different time points were observed. Results The levels of CK-MB,TNF-alpha and IL-1 beta increased significantly after the CLP operation. The levels of TNF-alpha and IL-1 beta was significantly relat-ed to CK-MB. After administering p38MAPK inhibitor and SB203580, the levels of TNF-alpha and IL-1 beta decreased significantly and the myocardial injury was alleviated. Condusion Excessive secretion of TNF-alpha and IL-1 beta are the main cause of myocardial injury in sepsis. The regulation of the p38MAPK pathway may protect myocardial injury.