To determine the role of hemoglobin( HB) induced heme oxygenase 1 (HO 1) in injured lungs caused by limb ischemia reperfusion (I/R) in rats. Methods: A rat model of ischemia in the hind limbs was made by clamping the ...To determine the role of hemoglobin( HB) induced heme oxygenase 1 (HO 1) in injured lungs caused by limb ischemia reperfusion (I/R) in rats. Methods: A rat model of ischemia in the hind limbs was made by clamping the infrarenal aorta with a microvascular clip, and lung injury occurre d after reperfusion. To induce the expression of HO 1 in the lungs, Hb was admi nistrated intraperitoneally at 16 hours before reperfusion. Northern blotting an d Western blotting were used to detect the expression of HO 1 in the lungs, and the carboxyhemoglobin (COHb) level in arterial blood was assayed. The effect of h emoglobin (Hb) on the injured lungs after limb I/R was determined by measuring t he changes of lung histology, polymorphonuclear (PMN) count, malondialdehyde (MD A) content and wet to dry weight ratio (W/D). Zinc protoporphyrin (ZnPP), an i nhibitor of HO, was used to determine whether HO 1 was induced by Hb after lun g injury. Results: Hb led to a significant increase in HO 1 mRNA and pro tein expression in the lungs, accompanied by the increase of COHb level in arter ial blood. Compared with the sham controls, the lung PMN count, MDA content and W/D significantly increased at 4 hours after limb I/R, which reversed by th e pretreatment with Hb at 16 hours before reperfusion. ZnPP blocked this protect ive role of Hb in the injured lungs. Conclusions: Hb can induce the lung HO 1 expression, which pla ys an important role in the defense against I/R induced lung injury in rats.展开更多
文摘To determine the role of hemoglobin( HB) induced heme oxygenase 1 (HO 1) in injured lungs caused by limb ischemia reperfusion (I/R) in rats. Methods: A rat model of ischemia in the hind limbs was made by clamping the infrarenal aorta with a microvascular clip, and lung injury occurre d after reperfusion. To induce the expression of HO 1 in the lungs, Hb was admi nistrated intraperitoneally at 16 hours before reperfusion. Northern blotting an d Western blotting were used to detect the expression of HO 1 in the lungs, and the carboxyhemoglobin (COHb) level in arterial blood was assayed. The effect of h emoglobin (Hb) on the injured lungs after limb I/R was determined by measuring t he changes of lung histology, polymorphonuclear (PMN) count, malondialdehyde (MD A) content and wet to dry weight ratio (W/D). Zinc protoporphyrin (ZnPP), an i nhibitor of HO, was used to determine whether HO 1 was induced by Hb after lun g injury. Results: Hb led to a significant increase in HO 1 mRNA and pro tein expression in the lungs, accompanied by the increase of COHb level in arter ial blood. Compared with the sham controls, the lung PMN count, MDA content and W/D significantly increased at 4 hours after limb I/R, which reversed by th e pretreatment with Hb at 16 hours before reperfusion. ZnPP blocked this protect ive role of Hb in the injured lungs. Conclusions: Hb can induce the lung HO 1 expression, which pla ys an important role in the defense against I/R induced lung injury in rats.
