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作 者:张红超[1] 于鲁峰[1] 李玲可[1] 杨玉红[1] Tao W.K Shi Chen
机构地区:[1]空军总医院心外科,北京100036 [2]美国西南医学中心胸心外科麻醉专业组
出 处:《中华实验外科杂志》2008年第10期1292-1293,共2页Chinese Journal of Experimental Surgery
摘 要: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-6knockout(IL-6KO,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±0.21ml/min,P〈0.05)与心爿E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。Objective By using the IL-6 deficiency mice,to study the role of IL-6 in comary endothelial cell (EC) injury during systemic inflammatory response syndrome (SIRS). Methods The TBSA bum 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 burn, acetylcholine ( 10s mol/L, 10 ml/ 5 min) was administered to K-H perfusion solution to study the change of cornary 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 stimula- tion 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 〈 0.05 ) 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 bum pathogenesis. But IL-6 deficiency seems to be advantageous for cardiac EC injury suffering from burn.
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