Objective： To investigate the effect of ischemic postconditioning （1PO） on acute lung ischemia-reperfusion （I/R） injury and the protein expression of haeme oxygenase-1 （HO-1）, a cytoprotective defense against o...Objective： To investigate the effect of ischemic postconditioning （1PO） on acute lung ischemia-reperfusion （I/R） injury and the protein expression of haeme oxygenase-1 （HO-1）, a cytoprotective defense against oxidative injury. Methods： After being anesthetized with chloralhydrate, forty-eight healthy SD rats were randomly divided into 6 groups （8 in each）： sham operation group （S group）; I/R group： left lung hilum was clamped for 40 minutes followed by 105 minutes of reperfusion; IPO group： left lung hilum was clamped for40 minutes and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion; Heroin （HM）＋ I/R group： heroin, an inducer of HO-1 was injected intraperitoneally at 40 μmol·kg^-1·day^-1 for two consecutive days prior to 40 minutes clamping of left lung hilum; ZnPPIX＋IPO group： zinc protoporphyrin IX, an inhibitor of HO-1 was injected intraperitoneally at 20 mg·kg^-1 24 hours prior to 40 minutes clamping of left lung hilum; and HM＋S group： HM was administered as in the HM＋I/R group without inducing lung I/R. Arterial partial pressure of oxygen （PaO2） and malondialdehyde （MDA） content in serum were assessed. The left lung was removed for determination of wet/dry lung weight ratio and expression of HO-1 protein by immuno-histochemical technique and for light microscopic examination. Results： The PaO2 was significantly lower in all the experimental groups compared with sham group （90 roan Hg ±11 mmHg）. However, the values of PaO2in IPO （81 mm Hg±7 mm Hg） and HM＋I/R （80 mm Hg±9 mm Hg） were higher than that in I/R （63 mm Hg±9 mm Hg） and ZnPPIX＋IPO （65 mm Hg±8 mm Hg） groups （P〈0.01）. The protein expression of HO- 1 in lung tissue was significantly increased in I/R group compared with S group （P〈0.01）. While the HO-1 protein expression was higher in IPO and HM＋I/R groups as compared with I/R group （P〈0.05, P〈0.01 ）. The lung wet/ dry （W/D） weight ratio and MDA content in serum were significantly increased in I/R group as compared with S or HM＋S groups （P〈0.01）, accompanied by severe lung tissue histological damage, which was attenuated either by IPO or by HM pretreatment （P〈0.01, IPO or HM＋I/R vs. I/R）. The protective effect of IPO was abolished by ZnPPIX. Conclusion： Ischemic postconditioning can attenuate the lung ischemia-reperfusion injury through upregulating the protein expression of HO-I that leads to reduced postischemic oxidative damage.展开更多
基金This project was supported by the National Natural Science Foundation of China （No.30672033）.
文摘Objective： To investigate the effect of ischemic postconditioning （1PO） on acute lung ischemia-reperfusion （I/R） injury and the protein expression of haeme oxygenase-1 （HO-1）, a cytoprotective defense against oxidative injury. Methods： After being anesthetized with chloralhydrate, forty-eight healthy SD rats were randomly divided into 6 groups （8 in each）： sham operation group （S group）; I/R group： left lung hilum was clamped for 40 minutes followed by 105 minutes of reperfusion; IPO group： left lung hilum was clamped for40 minutes and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion; Heroin （HM）＋ I/R group： heroin, an inducer of HO-1 was injected intraperitoneally at 40 μmol·kg^-1·day^-1 for two consecutive days prior to 40 minutes clamping of left lung hilum; ZnPPIX＋IPO group： zinc protoporphyrin IX, an inhibitor of HO-1 was injected intraperitoneally at 20 mg·kg^-1 24 hours prior to 40 minutes clamping of left lung hilum; and HM＋S group： HM was administered as in the HM＋I/R group without inducing lung I/R. Arterial partial pressure of oxygen （PaO2） and malondialdehyde （MDA） content in serum were assessed. The left lung was removed for determination of wet/dry lung weight ratio and expression of HO-1 protein by immuno-histochemical technique and for light microscopic examination. Results： The PaO2 was significantly lower in all the experimental groups compared with sham group （90 roan Hg ±11 mmHg）. However, the values of PaO2in IPO （81 mm Hg±7 mm Hg） and HM＋I/R （80 mm Hg±9 mm Hg） were higher than that in I/R （63 mm Hg±9 mm Hg） and ZnPPIX＋IPO （65 mm Hg±8 mm Hg） groups （P〈0.01）. The protein expression of HO- 1 in lung tissue was significantly increased in I/R group compared with S group （P〈0.01）. While the HO-1 protein expression was higher in IPO and HM＋I/R groups as compared with I/R group （P〈0.05, P〈0.01 ）. The lung wet/ dry （W/D） weight ratio and MDA content in serum were significantly increased in I/R group as compared with S or HM＋S groups （P〈0.01）, accompanied by severe lung tissue histological damage, which was attenuated either by IPO or by HM pretreatment （P〈0.01, IPO or HM＋I/R vs. I/R）. The protective effect of IPO was abolished by ZnPPIX. Conclusion： Ischemic postconditioning can attenuate the lung ischemia-reperfusion injury through upregulating the protein expression of HO-I that leads to reduced postischemic oxidative damage.
