CAJ | 학술논문

目的：观察正常肠淋巴液对内毒素休克小鼠肺、心、肝等器官损伤以及MAPK信号通路主要信号分子p38 MAPK、ERK1/2和JNK磷酸化水平的影响。方法：引流18只BALB/c雄性小鼠正常肠淋巴液，去除细胞成分后用于内毒素休克的干预。18只小鼠均分为假休克组、内毒素休克组与肠淋巴液干预组（ n＝6）；腹腔注射脂多糖（ LPS，35 mg/kg），复制小鼠内毒素休克模型；在LPS注射60 min后，淋巴液干预组小鼠经股动脉注射正常淋巴液（全血量的1/15）；整个实验过程监测平均动脉血压（MAP）；在腹腔注射LPS后6 h或相应时点，心尖穿刺取血，检测反映心肌和肝细胞损伤的生化指标；同时，留取固定位置的肺、心肌和肝组织，部分观察组织形态，部分检测p38 MAPK、ERK1/2和JNK的磷酸化水平。结果：内毒素休克组与肠淋巴液干预组小鼠在腹腔注射LPS后90 min多个时点的MAP显著低于假休克组，肠淋巴液干预组小鼠MAP在腹腔注射LPS后80 min、90 min、190 min、210 min、240 min、250 min、340 min、350 min和360 min显著高于内毒素休克组。假休克组小鼠肺、肝和心肌组织结构基本正常，内毒素休克组小鼠出现了一定的结构损伤，肠淋巴液干预组小鼠组织损伤较轻；内毒素休克组小鼠血浆AST、ALT和CK-MB活性高于假休克组，肠淋巴液干预组小鼠血浆CK-MB活性亦高于假休克组，AST和LDH-1活性低于内毒素休克组。注射LPS后6 h，小鼠肺组织p38 MAPK、ERK 1/2和JNK的磷酸化水平显著升高，心肌和肝组织的这些指标未见显著变化；输入正常肠淋巴液降低了内毒素休克小鼠肺组织p38 MAPK以及心肌组织p38 MAPK、ERK 1/2和JNK磷酸化水平。结论：输入正常肠淋巴液可减轻内毒素休克小鼠的器官损伤，降低肺组织p38 MAPK磷酸化水平。
목적：관찰정상장림파액대내독소휴극소서폐、심、간등기관손상이급MAPK신호통로주요신호분자p38 MAPK、ERK1/2화JNK린산화수평적영향。방법：인류18지BALB/c웅성소서정상장림파액，거제세포성분후용우내독소휴극적간예。18지소서균분위가휴극조、내독소휴극조여장림파액간예조（ n＝6）；복강주사지다당（ LPS，35 mg/kg），복제소서내독소휴극모형；재LPS주사60 min후，림파액간예조소서경고동맥주사정상림파액（전혈량적1/15）；정개실험과정감측평균동맥혈압（MAP）；재복강주사LPS후6 h혹상응시점，심첨천자취혈，검측반영심기화간세포손상적생화지표；동시，류취고정위치적폐、심기화간조직，부분관찰조직형태，부분검측p38 MAPK、ERK1/2화JNK적린산화수평。결과：내독소휴극조여장림파액간예조소서재복강주사LPS후90 min다개시점적MAP현저저우가휴극조，장림파액간예조소서MAP재복강주사LPS후80 min、90 min、190 min、210 min、240 min、250 min、340 min、350 min화360 min현저고우내독소휴극조。가휴극조소서폐、간화심기조직결구기본정상，내독소휴극조소서출현료일정적결구손상，장림파액간예조소서조직손상교경；내독소휴극조소서혈장AST、ALT화CK-MB활성고우가휴극조，장림파액간예조소서혈장CK-MB활성역고우가휴극조，AST화LDH-1활성저우내독소휴극조。주사LPS후6 h，소서폐조직p38 MAPK、ERK 1/2화JNK적린산화수평현저승고，심기화간조직적저사지표미견현저변화；수입정상장림파액강저료내독소휴극소서폐조직p38 MAPK이급심기조직p38 MAPK、ERK 1/2화JNK린산화수평。결론：수입정상장림파액가감경내독소휴극소서적기관손상，강저폐조직p38 MAPK린산화수평。
AIM:To observe the effects of normal mesenteric lymph (NML) on the lung, heart and liver inju-ries and the phosphorylation levels of p 38 mitogen-activated protein kinase ( MAPK) , extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) in the mice with endotoxic shock (ES).METHODS: The NML was drained form health male BALB/c mice for the intervention of ES after the removal of cellular constituent .Lipopolysaccha-ride (LPS, 35 mg/kg) was intraperitoneally injected into the mice for the establishment of ES model .After 60 min of LPS injection, the administration of NML (1/15 of whole blood volume) was performed through the femoral artery in NML +ES group.Meanwhile, the mean arterial pressure (MAP) was monitored during the experiment .At 6 h after intraperitoneal in-jection of LPS or the corresponding time point , blood samples were harvested from the heart through apical centesis for de-termination of the biochemical indexes to reflect myocardial and hepatocyte injuries .Simultaneously , the lung , heart and liver tissue specimens from a fixed location were harvested for the observation of histomorphology and the measurement of phosphorylation levels of p38 MAPK, ERK1/2 and JNK.RESULTS:Compared with sham shock (SS) group, MAP in ES group and NML+ES group remarkably decreased at multiple time points after intraperitoneal injection of LPS .However, MAP in NML+ES group at 80 min, 90 min, 190 min, 210 min, 240 min, 250 min, 340 min, 350 min, and 360 min were significantly increased compared with ES group .There were normal structures in the lung , liver and myocardium of the mice in SS group, while the morphological damages of these tissues appeared in ES group .Meanwhile, the damages were attenuated in the mice of NML +ES group.The activities of AST , ALT and CK-MB in the plasma in ES group were remark-ably higher than those in SS group .The CK-MB activity in NML+ES group was also increased compared with SS group , and the activities of AST and LDH-1 were lower than those in ES group .At 6 h after LPS injection , the phosphorylation levels of p38 MAPK, ERK1/2 and JNK in the lung tissues were remarkably increased .Meanwhile , no statistical difference of these indexes between the myocardial and hepatic tissues was observed .NML intervention decreased the phosphorylation levels of p38 MAPK in the lung tissues , and p38 MAPK, ERK1/2 and JNK in the myocardial tissues .CONCLUSION:The NML administration alleviates multi-organ injuries and reduces the phosphorylation level of p 38 MAPK in the lung tis-sues in the mice subjected to ES .