OBJECTIVE: To investigate the protective effects of the induction of heme oxygenase-1 (HO-1) on ischemia/reperfusion lung injury. METHODS: Forty Sprague-Dawley rats were randomly divided into four equal groups: sham group, lung ischemia/reperfusion injury (I/R) group, undergoing ligaturing of the left lung hilum for 30 minutes followed by reperfusion for 120 minutes; hemin group, undergoing intraperitoneal injection of hemin, an inducer of HO-1, 48 hours before the ligation and reperfusion; zinc protoporphyrin (ZnPP) group, undergoing intravenous injection of ZnPP, an inhibitor of heme oxygenase, 15 min after the ischemia-reperfusion; and sham operation group, undergoing sham operation. Two hours after the I/R arterial blood samples were collected and then the left lungs of the rats were taken out. Plasma tumor necrosis factor-alpha (TNF-alpha) and lung superoxide dismutase (SOD) activity were examined. Lung wet-to-dry weight (W/D) ratio was measured. The ultrastructure of the pulmonary alveoli and its capillaries were studied by using transmissional electronmicroscopy. RESULTS: The lung W/D ratio of the hemin group was 5.92 +/- 0.66, significantly lower than that of the I/R group (7.55 +/- 0.66, P < 0.01), and that of the ZnPP group (7.34 +/- 0.39, P < 0.01). The SOD activity of the hemin group was 6.5 +/- 0.6 U/mg protein, significantly higher than those of the I/R group and ZnPP group (2.8 +/- 0.4 U/mg protein and 3.0 +/- 0.4 U/mg protein respectively, both P < 0.01). The plasma TNF-alpha was 180.36 +/- 12.46, significantly lower than those of the I/R and ZnPP groups (452.26 +/- 22.59 and 438.59 +/- 30.26 respectively, both P < 0.01). Transmissional electronmicroscopy showed that the microscopic structure of the sham group was normal and that the pathological changes of hemin group were milder then those of the T/R and ZnPP groups. CONCLUSION: The induction of heme oxygenase-1 can protect effectively the lesion of lung pathology in ischemia reperfusion in vivo.
OBJECTIVE: To investigate the protective effects of the induction of heme oxygenase-1 (HO-1) on ischemia/reperfusion lung injury. METHODS: Forty Sprague-Dawley rats were randomly divided into four equal groups: sham group, lung ischemia/reperfusion injury (I/R) group, undergoing ligaturing of the left lung hilum for 30 minutes followed by reperfusion for 120 minutes; hemin group, undergoing intraperitoneal injection of hemin, an inducer of HO-1, 48 hours before the ligation and reperfusion; zinc protoporphyrin (ZnPP) group, undergoing intravenous injection of ZnPP, an inhibitor of heme oxygenase, 15 min after the ischemia-reperfusion; and sham operation group, undergoing sham operation. Two hours after the I/R arterial blood samples were collected and then the left lungs of the rats were taken out. Plasma tumor necrosis factor-alpha (TNF-alpha) and lung superoxide dismutase (SOD) activity were examined. Lung wet-to-dry weight (W/D) ratio was measured. The ultrastructure of the pulmonary alveoli and its capillaries were studied by using transmissional electronmicroscopy. RESULTS: The lung W/D ratio of the hemin group was 5.92 +/- 0.66, significantly lower than that of the I/R group (7.55 +/- 0.66, P < 0.01), and that of the ZnPP group (7.34 +/- 0.39, P < 0.01). The SOD activity of the hemin group was 6.5 +/- 0.6 U/mg protein, significantly higher than those of the I/R group and ZnPP group (2.8 +/- 0.4 U/mg protein and 3.0 +/- 0.4 U/mg protein respectively, both P < 0.01). The plasma TNF-alpha was 180.36 +/- 12.46, significantly lower than those of the I/R and ZnPP groups (452.26 +/- 22.59 and 438.59 +/- 30.26 respectively, both P < 0.01). Transmissional electronmicroscopy showed that the microscopic structure of the sham group was normal and that the pathological changes of hemin group were milder then those of the T/R and ZnPP groups. CONCLUSION: The induction of heme oxygenase-1 can protect effectively the lesion of lung pathology in ischemia reperfusion in vivo.