Conclusion: COPD have chronic inflammation, the increase of oxidation and decrease of antioxidation activity of α_1-AT and unbalance of protease and antiprotease might play an important role in smoking-induced diseases. 结论:慢性阻塞性肺疾病存在慢性炎症,氧化作用强,抗氧化能力弱,α1-AT活性减低。吸烟影响机体的抗氧化能力,影响肺的蛋白酶/抗蛋白酶平衡,对COPD的发生、发展有重要作用。
Conclusion The lower expression of TIMP-2, which leads to the imbalance between protease and antiprotease, may be associated with the pathogenesis of COPD. Smoking may play an important role in the expression of TIMP-2 mRNA. 结论TIMP-2mRNA表达降低,而导致蛋白酶-抗蛋白酶失衡可能与COPD的发生相关,而吸烟是影响TIMP-2mRNA表达的较为重要的因素。
Experimental Studies on Protease Antiprotease Balance of Rats Exposed to Hyperoxia 氧中毒大鼠蛋白酶抗蛋白酶平衡状态的实验研究
Conclusion In ALI patients, the activity of serum NE was significantly elevated, but the activity of α_1-AT was reduced. There was an imbalance between protease and antiprotease. The activity of serum NE was significantly related to the severity and prognosis of ALI patients. 结论ALI患者的NE活性明显升高,α1AT活性显著降低,出现蛋白酶抗蛋白酶失衡,而且血清NE活性水平与患者的肺损伤严重程度和预后密切相关。
Objective To clone human new type antiprotease protector ( elafin) gene cDNA, and construct its highly efficient eukaryotic expression vector. 目的克隆人肺新型抗蛋白酶性保护因子elafin基因cDNA,构建该基因的真核高效表达载体。
However, the pathogenesis of COPD have not yet clarified, Currently that may be related to the chronic airway inflammation 、 protease and antiprotease imbalance 、 oxidation and antioxidant imbalance mechanisms, In which Chronic airway inflammation mechanism was concerned. 目前COPD的发病机制仍未阐明,目前认为可能和气道的慢性炎症、蛋白酶与抑蛋白酶失衡、氧化与抗氧化失衡等机制有关。其中气道慢性非特异性炎症机制备受关注。