CAJ | 학술논문

目的应用基因敲除小鼠模型研究白细胞介素(IL)-6在这一损伤过程中对内皮细胞的损伤作用及其机制.方法 IL-6 knockout(IL-6 KO,C57BL/6J-116tmlKopf,实验组)小鼠与其野生型小鼠C57BL/6J(对照组)分别给予40%烧伤,用Langendorff离体工作心模型观察烧伤后鼠心心功能及冠脉流量的变化,并观察内皮细胞对乙酰胆碱的反应性,用HE和Tunel染色观察心肌血管及其内皮细胞的变化.结果在非烧伤应急情况下,对照组与实验组的冠脉流量、心排出量及对乙酰胆碱刺激的反应均无明显差异,病理学差异无统计学意义.但在烧伤后,对照组冠脉流量(1.94±0.17比2.32±0.21 mL/min,P＜0.05)与心排量(3.7±0.3)比(7.5±0.4)ml/min,P＜0.05)均显著减少,对乙酰胆碱刺激的反应显著低于实验组(2.34±0.23)比(2.88±0.26);(5.0±0.4)比(8.4±0.4),P＜0.05);病理学上对照组血管内皮肿胀、排列紊乱及内皮细胞凋亡现象.结论循环血液中IL-6对内皮细胞的损伤作用可能是其心功能抑制的始动环节.
목적 응용기인고제소서모형연구백세포개소(IL)-6재저일손상과정중대내피세포적손상작용급기궤제.방법 IL-6 knockout(IL-6 KO,C57BL/6J-116tmlKopf,실험조)소서여기야생형소서C57BL/6J(대조조)분별급여40%소상,용Langendorff리체공작심모형관찰소상후서심심공능급관맥류량적변화,병관찰내피세포대을선담감적반응성,용HE화Tunel염색관찰심기혈관급기내피세포적변화.결과 재비소상응급정황하,대조조여실험조적관맥류량、심배출량급대을선담감자격적반응균무명현차이,병이학차이무통계학의의.단재소상후,대조조관맥류량(1.94±0.17비2.32±0.21 mL/min,P＜0.05)여심배량(3.7±0.3)비(7.5±0.4)ml/min,P＜0.05)균현저감소,대을선담감자격적반응현저저우실험조(2.34±0.23)비(2.88±0.26);(5.0±0.4)비(8.4±0.4),P＜0.05);병이학상대조조혈관내피종창、배렬문란급내피세포조망현상.결론 순배혈액중IL-6대내피세포적손상작용가능시기심공능억제적시동배절.
Objective By using the IL-6 deficiency mice,to study the role of IL-6 in cornary endothelial cell (EC) injury during systemic inflammatory response syndrome (SIRS). Methods The TBSA burn mice model was used to simulate the clinicopathological process. IL-6 knock out mice (IL-6 KO, C57BL/6J-I16tmlKopf) were used for evaluating the role of IL-6 in this process. The wild type C56/BL6 male and IL-6 knock out mice were burned in 40% respectively. In addition to observation of cornary flow (CF) and cardiac function with Langendorff method in 24 h after bum, acetyleholine ( 10.5 tool/L, 10 ml/ 5 rain) was administered to K-H perfusion solution to study the change of comary flow (CF). At the final, pathological morphologic changes were analyzed with H&E and Tunel stain. Results Without burn, there were no difference between the two groups in cornary flow, cardiac output (CO) and acetylcholine stimulation as well as pathological changes. However, there was significant difference between the control group and knockout group in the CF ( 1.94 ±0.17 vs 2.32 ± 0.21 ml/min, P ＜ 0.05 ) and CO (3.7 ± 0.3 vs 7.5 ± 0.4 ml/min, P ＜ O. 05 ) after burn. There also was significant different response to acetylcholine (CF:2.34 ±0.23 vs 2.88 ±0.26;CO:5.0 ±0.4 vs 8.4 ± 0.4,P ＜0.05). In IL-6 knock out mice there was milder EC injury and appotosis in heart pathology. Conclusion The cytokine IL-6 is a risk factor in burn pathogenesis. But IL-6 deficiency seems to be advantageous for cardiac EC injury suffering from burn.