Objective： To observe the role and mechanism of CO- releasing molecule （CORM）-2 in lung injury induced by ischemia-reperfusion （IR） of hind limbs in rats. Methods： Arat model of lung injury induced by IR of hind...Objective： To observe the role and mechanism of CO- releasing molecule （CORM）-2 in lung injury induced by ischemia-reperfusion （IR） of hind limbs in rats. Methods： Arat model of lung injury induced by IR of hind limbs was established. A total of 40 Sprague Dawley （SD） rats were randomly divided into 5 groups （n = 8）： sham, sham ＋ CORM-2, IR, IR ＋ CORM-2 and IR ＋ dimethyl sulfoxide （DMSO）. Rats in the IR group received hind limb ischemia for 2 hours and reperfusion for 2 hours, rats in the sham group underwent sham surgery without infrarenal aorta occlusion, rats in the IR＋CORM-2 group and in the sham ＋ CORM-2 group were given CORM-2 （10 μmol/kg intravenous bolus） 5 minutes before reperfusion or at the corresponding time points, while rats in the IR ＋ DMSO group was treated with the same dose of vehicle （DMSO） at the same time. The lung tissue structure, polymorphonuclear neutrophil （PMN） count, wet-to-dry weight ratio （W/D）, malondialdehyde （MDA） content, myeloperoxidase （MPO） activity, intercellular adhesion molecule- 1 （ICAM- 1）expression, I κBα degradation and nuclear factor （NF）-κB activity in the lungs were assessed. Results： As compared with the sham group, lung PMNs number, W/D, MDA content, MPO activity, ICAM-1 expression and NF- κB activity significantly increased in the IR group, but the level of I κBα decresed （P〈0.01）. Compared with the IR group, lung PMNs number, W/D, MDA content, MPO activity and ICAM- 1 expression significantly decreased in the IR＋COMR-2 group （P〈0.01）, while the level of IκBα increased. Conclusions： These data demonstrate that CORM-2 attenuates limb IR-induced lung injury through inhibiting ICAM-1 protein expression, NF-κB pathway and the leu- kocytes sequestration in the lungs following limb IR in rats, suggesting that CORM-2 may be used as a therapeutic agent against lung injury induced by limb IR.展开更多
目的:探讨人重组促红细胞生成素(rHuEPO)对大鼠缺血/再灌注(I/R)心肌细胞的保护作用.方法:常规酶解法获得成年大鼠心室肌细胞,用氰化钠/乳酸钠灌注造成细胞化学缺氧以模拟缺血.缺血15 m in后以台氏液或台氏液加rHuEPO复氧模拟再灌注,用...目的:探讨人重组促红细胞生成素(rHuEPO)对大鼠缺血/再灌注(I/R)心肌细胞的保护作用.方法:常规酶解法获得成年大鼠心室肌细胞,用氰化钠/乳酸钠灌注造成细胞化学缺氧以模拟缺血.缺血15 m in后以台氏液或台氏液加rHuEPO复氧模拟再灌注,用可视化动缘探测系统同步检测rHuEPO对单个I/R心室肌细胞收缩力和钙瞬变的影响.结果:发现rHuEPO使再灌注后心室肌细胞肌小节最大收缩幅度、最大缩短速率、最大复长速率以及Ca2+荧光比率增大,使Ca2+达峰值时程、舒张期Ca2+减少50%时程减少(P<0.05,n=10,来自8个心脏).结论:rHuEPO可促进I/R心室肌细胞收缩及钙瞬变的恢复而发挥其保护作用.展开更多
基金This project was supported by the National Natural Science Foundation of China （No. 30271337）.
文摘Objective： To observe the role and mechanism of CO- releasing molecule （CORM）-2 in lung injury induced by ischemia-reperfusion （IR） of hind limbs in rats. Methods： Arat model of lung injury induced by IR of hind limbs was established. A total of 40 Sprague Dawley （SD） rats were randomly divided into 5 groups （n = 8）： sham, sham ＋ CORM-2, IR, IR ＋ CORM-2 and IR ＋ dimethyl sulfoxide （DMSO）. Rats in the IR group received hind limb ischemia for 2 hours and reperfusion for 2 hours, rats in the sham group underwent sham surgery without infrarenal aorta occlusion, rats in the IR＋CORM-2 group and in the sham ＋ CORM-2 group were given CORM-2 （10 μmol/kg intravenous bolus） 5 minutes before reperfusion or at the corresponding time points, while rats in the IR ＋ DMSO group was treated with the same dose of vehicle （DMSO） at the same time. The lung tissue structure, polymorphonuclear neutrophil （PMN） count, wet-to-dry weight ratio （W/D）, malondialdehyde （MDA） content, myeloperoxidase （MPO） activity, intercellular adhesion molecule- 1 （ICAM- 1）expression, I κBα degradation and nuclear factor （NF）-κB activity in the lungs were assessed. Results： As compared with the sham group, lung PMNs number, W/D, MDA content, MPO activity, ICAM-1 expression and NF- κB activity significantly increased in the IR group, but the level of I κBα decresed （P〈0.01）. Compared with the IR group, lung PMNs number, W/D, MDA content, MPO activity and ICAM- 1 expression significantly decreased in the IR＋COMR-2 group （P〈0.01）, while the level of IκBα increased. Conclusions： These data demonstrate that CORM-2 attenuates limb IR-induced lung injury through inhibiting ICAM-1 protein expression, NF-κB pathway and the leu- kocytes sequestration in the lungs following limb IR in rats, suggesting that CORM-2 may be used as a therapeutic agent against lung injury induced by limb IR.
文摘目的:探讨人重组促红细胞生成素(rHuEPO)对大鼠缺血/再灌注(I/R)心肌细胞的保护作用.方法:常规酶解法获得成年大鼠心室肌细胞,用氰化钠/乳酸钠灌注造成细胞化学缺氧以模拟缺血.缺血15 m in后以台氏液或台氏液加rHuEPO复氧模拟再灌注,用可视化动缘探测系统同步检测rHuEPO对单个I/R心室肌细胞收缩力和钙瞬变的影响.结果:发现rHuEPO使再灌注后心室肌细胞肌小节最大收缩幅度、最大缩短速率、最大复长速率以及Ca2+荧光比率增大,使Ca2+达峰值时程、舒张期Ca2+减少50%时程减少(P<0.05,n=10,来自8个心脏).结论:rHuEPO可促进I/R心室肌细胞收缩及钙瞬变的恢复而发挥其保护作用.
