CAJ | 학술논문

目的通过抑制MAPK通路活化,观察其对脓毒症大鼠组织和血清诱导型一氧化氮合成酶（iN-OS）及一氧化氮（NO）合成的影响以及循环变化.方法大鼠脓毒症模型采用经典的盲肠结扎穿孔术（cecalligation puncture,CLP）,将SD大鼠随机分为正常对照组、假手术组、CLP脓毒症组和SB203580治疗组.采集组织和血清并测定组织iNOSmRNA表达水平,NO检测试剂盒（酶法）检测组织和血清NO含量;同时分别监测上述各时间点的脉搏和平均动脉压.结果与正常组大鼠相比,CLP后各时间点脓毒症大鼠肺、血管和血清iNOS mRNA、NO含量均升高明显;而MAP下降明显、脉搏明显升高（P〈0.05,P〈0.01）.治疗组与CLP组相应时间点相比,iNOSmRNA表达在肺和血管多个时间点降低;而肺和血管及血清NO含量下降;血压和脉搏均显著好转（P〈0.05,P〈0.01）.相关分析显示：血管和肺组织iNOSmRNA与NO的相关系数分别是0.75和0.74;肺、血管组织iNOS mRNA与血清NO的相关系数分别是0.69和0.65（P〈0.05）,MAP与血管、肺和血清NO的相关系数分别是-0.85、-0.86和-0.90（P〈0.05）.结论抑制MAPK通路活化可抑制脓毒症大鼠血浆和组织iNOSmRNA及NO合成,并改善循环功能.
목적통과억제MAPK통로활화,관찰기대농독증대서조직화혈청유도형일양화담합성매（iN-OS）급일양화담（NO）합성적영향이급순배변화.방법대서농독증모형채용경전적맹장결찰천공술（cecalligation puncture,CLP）,장SD대서수궤분위정상대조조、가수술조、CLP농독증조화SB203580치료조.채집조직화혈청병측정조직iNOSmRNA표체수평,NO검측시제합（매법）검측조직화혈청NO함량;동시분별감측상술각시간점적맥박화평균동맥압.결과여정상조대서상비,CLP후각시간점농독증대서폐、혈관화혈청iNOS mRNA、NO함량균승고명현;이MAP하강명현、맥박명현승고（P〈0.05,P〈0.01）.치료조여CLP조상응시간점상비,iNOSmRNA표체재폐화혈관다개시간점강저;이폐화혈관급혈청NO함량하강;혈압화맥박균현저호전（P〈0.05,P〈0.01）.상관분석현시：혈관화폐조직iNOSmRNA여NO적상관계수분별시0.75화0.74;폐、혈관조직iNOS mRNA여혈청NO적상관계수분별시0.69화0.65（P〈0.05）,MAP여혈관、폐화혈청NO적상관계수분별시-0.85、-0.86화-0.90（P〈0.05）.결론억제MAPK통로활화가억제농독증대서혈장화조직iNOSmRNA급NO합성,병개선순배공능.
Objective To investigate the effects of p38 mitogen activated protein kinase on synthesis of inducible nitric oxide synthase（iNOS）and nitric oxide（NO）in infectious shock rats.Methods SD rats were randomly divided into normal control,sham operation,cecal ligation puncture（CLP）,and inhibitor of p38MAPK（SB203580）treatment groups Rats in.CLP and treatment groups were established into sepsis model induced by CLP,and at 2,6,24 h after CLP,the rats were sacrificed.The vascular,pulmonary tissues and serum samples of all rats were harvested to determine iNOS mRNA expression levels by reverse transcription polymerase chain reaction and NO content respectively.Meanwhile,the mean arterial pressure（MAP）and pulse were monitored.Results Compared with that of normal control,iNOS mRNA and NO levels in vascular,pulmonary tissues and serum at 2,6 and 24 h following CLP significantly increased respectively,and MAP fell notably and pulse increased（P0.05 or 0.01）.SB203580 treatment reduced iNOS mRNA and NO levels markedly at 2 or 6 h after CLP,meanwhile,MAP and pulse deteriorated by sepsis were also ameliorated（P0.05 or 0.01）.Conclusion Inhibiting the activation of MAPK pathway can decrease tissues and serum iNOS mRNA and NO expressions in infectious shock rats and can ameliorate the circulatory function deteriorated by sepsis.