实验性肝硬化大鼠肺脏血红素氧合酶的表达与定位

Expression and location of heme oxygenase in the lung of experimental cirrhotic rats

目的 观察肝硬化大鼠肺脏中血红素氧合酶(HO)的表达与定位,探讨血红素氧合酶-内源性一氧化碳在肝硬化时肺脏病变的作用。方法 建立四氯化碳肝硬化模型,应用免疫组织化学法和免疫印迹法对肝硬化大鼠和正常对照大鼠肺脏中血红素氧合酶的表达与定位进行比较。 结果 肝硬化模型制备成功。正常对照组大鼠HO-1在肺组织的表达较低,而肝硬化组大鼠的肺组织中HO-1蛋白表达明显增高(0.062±0.021与0.185±0.044,t=11.24,P<0.01 ;0与5 294.92±46.02,t=11.45,P<0.01),主要在血管和支气管的平滑肌细胞,内皮细胞及气道上皮细胞的胞浆内,而HO-2在两组大鼠的肺组织中表达差异无显著性(0.218±0.048与0.238±0.079,t=0.99,P>0.05; 5984.17±35.64与6040.75±42.43,t=0.02,P>0.05)。 结论 血红素氧合酶-内源性一氧化碳途径可能在肝硬化肺脏病变的发生机制中起一定的作用。

Objective To observe the function of heme oxygenase (HO) in the lung damage in hepatic cirrhosis rats. Methods Liver cirrhosis model rats were made by CCl4. Lung samples taken from normal and cirrhotic rats were examined for HO-1 and HO-2 protein and expression distribution with immunohistochemical staining and western blot. Results Liver cirrhosis model rats were successfully constructed. There was a notable increase of HO-1 staining (0.062±0.021 vs 0.185±0.044, t = 11.24, P < 0.01) and protein expression(0 vs 5 294.92±46.02, t = 11.45, P < 0.01) in both vascular and bronchial smooth muscle cells and endothelium in cirrhotic rats, however, no statistical difference of HO-2 between cirrhotic and normal rats was observed. Conclusion The HO-CO pathway is probably involved in the pathogenesis of lung damage in hepatic cirrhosis rats.