Effects of Ischemic Postconditioning on Inflammatory Response in Ischemia-Reperfusion Injury of Rat Lungs in Vivo_Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

Authors：

DUAN Mingke , MA Limin , LAN Junbin , WU Yigen , XIONG Wei , GAO Yizhe , XU Shengshui.

1. Department of Thoracic and Cardiovascular Surgery，No. 2 Peoples’ Hospital of Xiamen，Xiamen 361021，Fujian，P. R. China;;
2. Department of Thoracic and Cardiovascular Surgery，Second Affiliated Hospital of Medical College，Shantou University，Shantou 515041，Guangdong，P. R. China;

Corresponding author：

Keywords：

Ischemia-reperfusion injury; 　Ischemic postconditioning; 　Interleukin-10; 　Soluble intercelleur adhension moleucule-1

DOI：

10.7507/1007-4848.20130215

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Objective To investigate the effects of ischemic postconditioning （IPO） on inflammatory response inischemia-reperfusion （IR） injury of rat lungs in vivo. Methods Forty SD rats were randomly divided into 5 groups inclu-ding a sham surgery group （S group），a 30-minute IR group （I/R-30 group），a 120-minute IR group（IR-120 group），a 30-minute IPO group （IPO-30 group），and a 120-minute IPO group （IPO-120 group）. There were 8 rats in each group. All therats received left thoracotomy after anesthesia. In the sham surgery group，a line was only placed around the left hilum butnot fastened. In the I/R-30 group and I/R-120 group，a line was fastened to block the blood flow of the left lung for 1 hour，then loosened for reperfusion for 30 minutes and 120 minutes respectively. In the IPO-30 group and IPO-120 group，afterblocking the blood flow of the left lung for 1 hour，the left hilum was fastened for 10 seconds and loosened for 10 seconds（repeating 3 times for 1 minute），then the line was loosened for 30 minutes and 120 minutes respectively. The levels of interleukin-10 （IL-10） in lung tissues and soluble intercellular adhesion molecule-1 （sICAM-1） in plasma were measured. Histopathological changes of lung tissues were observed and diffuse alveolar damage （DAD） scores was calculated.Results The levels of plasma sICAM-1 in the I/R-30 group and I/R-120 group were significantly higher than that of S group ［（2.140±0.250）μg/L vs. （0.944±0.188）μg/L，P=0.003；（2.191±0.230）μg/L vs. （0.944±0.188）μg/L，P=0.003］. IL-10levels in lung tissues in the I/R-30group and I/R-120 group were also significantly higher than that of S group［（15.922±0.606）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.037；（17.421±1.232）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.042］. Pathologic lesions of lung tissues in the I/R-30 group and I/R-120 group were more severe than that of S group. After IPO, plasma sICAM-1 levels in the IPO-30 group and IPO-120 group were significantly lower than those in the I/R-30group and I/R-120 group respectively ［（1.501±0.188）μg/L vs.（2.140±0.250）μg/L，P=0.038；（1.350±0.295）μg/L vs.（2.191±0.230）μg/L，P=0.005］. IL-10 levels in lung tissues in the IPO-30 group and IPO-120 group were significantly higherthan those in the I/R-30 group and I/R-120 group respectively ［（20.950±1.673）pg/mg pro vs.（15.922±0.606）pg/mgpro，P=0.008；（25.334±1.173）pg/mg pro vs.（17.421±1.232）pg/mg pro，P=0.006］. DAD scores in the IPO-30 group andIPO-120 group were significantly lower than those in the I/R-30 group and I/R-120 group respectively ［6.8±1.4 vs. 11.5±1.9，P=0.007；7.5±1.6 vs. 13.2±1.7，P=0.005］. Pathological lesions of the lung tissues of IPO groups were less severe than those of I/R groups. Conclusion IPO can attenuate IR injury by inhibiting inflammatory response in rat lungs.

Citation： DUAN Mingke,MA Limin,LAN Junbin,WU Yigen,XIONG Wei,GAO Yizhe,XU Shengshui.. Effects of Ischemic Postconditioning on Inflammatory Response in Ischemia-Reperfusion Injury of Rat Lungs in Vivo. Chinese Journal of Clinical Thoracic and Cardiovascular Surgery, 2013, 20(6): 705-709. doi: 10.7507/1007-4848.20130215 Copy

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2.	Ng CS， Wan S， Arifi AA， et al. Inflammatory response to pulmonaryischemia-reperfusion injury. Surg Today， 2006， 36 （3）：205-214.
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7.	Selzner N， Boehnert M， Selzner M. Preconditioning， postconditi-oning， and remote conditioning in solid organ transplantation：basic mechanisms and translational applications. Transplant Rev （Orlando），2012， 26 （2）：115-124.
8.	Zhu SB， Liu Y， Zhu Y， et al. Remote preconditioning， perconditioning， and post-conditioning：a comparative study of their cardioprotective properties in rat models. Clinics （Sao Paulo）， 2013， 68 （2）：263-268.
9.	Kong Y， Rogers MR， Qin X. Effective neuroprotection by ischemic postconditioning is associated with a decreased expression of RGMa and inflammation mediators in ischemic rats. Neurochem Res， 2013， 38 （4）：815-825.
10.	Cheng CH， Lin HC， Lai IR， et al. Ischemic postconditioning atten-uate reperfusion injury of small intestine：impact of mitochondrial permeability transition. Transplantation， 2013， 95 （4）：559-565.
11.	刘洪端，刘立明. 缺血后处理的研究进展. 中国胸心血管外科临床杂志， 2012， 19 （3）：309-311.
12.	den Hengst WA， Gielis JF， Judy Y， et al. Lung ischemia-reperfusion injury：a molecular and clinical view on a complex pathophysiological process. Am J Physiol Heart Circ Physiol， 2010， 299 （5）：H1283-H1299.
13.	杨波，张志培，姜鹏，等. 褪黑素对大鼠肠缺血再灌注肺损伤及N-myc下游调节基因2表达的影响. 中国呼吸与危重监护杂志， 2013， 12 （1）：61-64.
14.	蒲江涛，刘伦旭，余南彬，等. 参附注射液对兔移植肺缺血-再灌注损伤的保护作用. 中国胸心血管外科临床杂志， 2010， 17 （3）：257-259.
15.	鲁建军，姚达，秦存伟，等. 缺血后处理对犬肺移植术后早期炎症反应的影响. 中山大学学报：医学科学版， 2009， 30 （5）：547-550.
16.	Vinten-Johansen J， Jiang R， Reeves JG， et al. Inflammation， proin-flammatory mediators and myocardial ischemia-reperfusion injury. Hematol Oncol Clin North Am， 2007， 21 （1）：123-145.
17.	任大宾，孙仁宇. 白介素10的抗炎功能及其分子机制. 国外医学：呼吸系统分册， 2005， 25 （3）：175-178.
18.	蓝杨，李理，袁伟锋，等. IL-10对脂多糖诱导Ana-1细胞的MyD88/核因子κB活性影响的研究. 中国呼吸与危重监护杂志， 2010， 9 （3）：243-245.
19.	Farivar AS， Krishnadasan B， Naidu BV， et al. Endogenous interleukin 4 and interleukin-10 regulate experimental lung ischemia reper-fusion injury. Ann Thorac Surg， 2003， 76 （1）：253-259.
20.	Kabay B， Aytekin FO， Aydin C， et al. Interleukin-10 gene therapy attenuates pulmonary tissue injury caused by mesenteric ischemia-reperfusion in a mouse model. Tohoku J Exp Med， 2005， 207 （2）：133-142.
21.	Lutz J， Thürme K， Heemann U. Anti-inflammatory treatment strategies for ischemia-reperfusion injury in transplantation. J Inflam （Lond）， 2010， 7：27-34.
22.	刘东，曾邦雄，张诗海，等. PPAR受体激动剂抑制急性肺损伤大鼠肺脏粘附分子和趋化因子的表达. 中国病理生理杂志， 2006， 22 （8）：1558-1561.
23.	Witkowska1 AM， Borawska MH. Soluble intercellular adhesion molecule-1 （sICAM-1）：an overview. Eur Cytokine Netw， 2004， 15 （2）：91-98.
24.	范丽丽，于湘友. 乌司他丁对体外循环患者细胞黏附分子浓度影响及对肺损伤保护作用. 中华实用诊断与治疗杂志， 2010， 24 （2）：136-138.

1. 　Fiser SM， Tribble CG， Long SM， et al. Ischemia-reperfusion injury after lung transplantation increases risk of late bronchiolitis obliterans syndrome. Ann Thorac Surg， 2002， 73 （4）：1041-1048.
2. 　Ng CS， Wan S， Arifi AA， et al. Inflammatory response to pulmonaryischemia-reperfusion injury. Surg Today， 2006， 36 （3）：205-214.
3. 　Seibert AF， Haynes J， Taylor A. Ischemia-reperfusion injury in the isolated rat lung Role of flow and endogenous leukocytes. Am Rev Raspir Dis， 1993， 147 （2）：270-275.
4. 　Heusch G. Postconditioning：old wine in a new bottle? J Am Coll Cardio， 2004， 44 （5）：1111-1112.
5. 　Quintel M， Heine M， Hirschl RB， et al. Effects of partial liquid ventilation on lung injury in a model of acute respiratory failure：a histologic and morphometric analysis. Crit Care Med， 1998， 26 （5）：833-843.
6. 　Beręsewicz A. Endogenous cardioprotective mechanisms - what is it about and how does it work ? Kardiol Pol， 2011， 69 （Suppl 3）：59-66.
7. 　Selzner N， Boehnert M， Selzner M. Preconditioning， postconditi-oning， and remote conditioning in solid organ transplantation：basic mechanisms and translational applications. Transplant Rev （Orlando），2012， 26 （2）：115-124.
8. 　Zhu SB， Liu Y， Zhu Y， et al. Remote preconditioning， perconditioning， and post-conditioning：a comparative study of their cardioprotective properties in rat models. Clinics （Sao Paulo）， 2013， 68 （2）：263-268.
9. 　Kong Y， Rogers MR， Qin X. Effective neuroprotection by ischemic postconditioning is associated with a decreased expression of RGMa and inflammation mediators in ischemic rats. Neurochem Res， 2013， 38 （4）：815-825.
10. 　Cheng CH， Lin HC， Lai IR， et al. Ischemic postconditioning atten-uate reperfusion injury of small intestine：impact of mitochondrial permeability transition. Transplantation， 2013， 95 （4）：559-565.
11. 　刘洪端，刘立明. 缺血后处理的研究进展. 中国胸心血管外科临床杂志， 2012， 19 （3）：309-311.
12. 　den Hengst WA， Gielis JF， Judy Y， et al. Lung ischemia-reperfusion injury：a molecular and clinical view on a complex pathophysiological process. Am J Physiol Heart Circ Physiol， 2010， 299 （5）：H1283-H1299.
13. 　杨波，张志培，姜鹏，等. 褪黑素对大鼠肠缺血再灌注肺损伤及N-myc下游调节基因2表达的影响. 中国呼吸与危重监护杂志， 2013， 12 （1）：61-64.
14. 　蒲江涛，刘伦旭，余南彬，等. 参附注射液对兔移植肺缺血-再灌注损伤的保护作用. 中国胸心血管外科临床杂志， 2010， 17 （3）：257-259.
15. 　鲁建军，姚达，秦存伟，等. 缺血后处理对犬肺移植术后早期炎症反应的影响. 中山大学学报：医学科学版， 2009， 30 （5）：547-550.
16. 　Vinten-Johansen J， Jiang R， Reeves JG， et al. Inflammation， proin-flammatory mediators and myocardial ischemia-reperfusion injury. Hematol Oncol Clin North Am， 2007， 21 （1）：123-145.
17. 　任大宾，孙仁宇. 白介素10的抗炎功能及其分子机制. 国外医学：呼吸系统分册， 2005， 25 （3）：175-178.
18. 　蓝杨，李理，袁伟锋，等. IL-10对脂多糖诱导Ana-1细胞的MyD88/核因子κB活性影响的研究. 中国呼吸与危重监护杂志， 2010， 9 （3）：243-245.
19. 　Farivar AS， Krishnadasan B， Naidu BV， et al. Endogenous interleukin 4 and interleukin-10 regulate experimental lung ischemia reper-fusion injury. Ann Thorac Surg， 2003， 76 （1）：253-259.
20. 　Kabay B， Aytekin FO， Aydin C， et al. Interleukin-10 gene therapy attenuates pulmonary tissue injury caused by mesenteric ischemia-reperfusion in a mouse model. Tohoku J Exp Med， 2005， 207 （2）：133-142.
21. 　Lutz J， Thürme K， Heemann U. Anti-inflammatory treatment strategies for ischemia-reperfusion injury in transplantation. J Inflam （Lond）， 2010， 7：27-34.
22. 　刘东，曾邦雄，张诗海，等. PPAR受体激动剂抑制急性肺损伤大鼠肺脏粘附分子和趋化因子的表达. 中国病理生理杂志， 2006， 22 （8）：1558-1561.
23. 　Witkowska1 AM， Borawska MH. Soluble intercellular adhesion molecule-1 （sICAM-1）：an overview. Eur Cytokine Netw， 2004， 15 （2）：91-98.
24. 　范丽丽，于湘友. 乌司他丁对体外循环患者细胞黏附分子浓度影响及对肺损伤保护作用. 中华实用诊断与治疗杂志， 2010， 24 （2）：136-138.

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Effects of Ischemic Postconditioning on Inflammatory Response in Ischemia-Reperfusion Injury of Rat Lungs in Vivo

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