摘要
目的:观察水蛭对肺纤维化大鼠纤溶酶原激活物抑制因子-1(Plasminogen activator inhibitor-1,PAI-1)的作用,并探讨其机制。方法:采用气管内注入博莱霉素(BLM)制作大鼠肺纤维化模型,造模后随机分为模型组(MD组,生理盐水6 ml/d灌胃),水蛭组[HD组,水蛭粉4 g/(kg.d)灌胃],另设鼠龄、体重相匹配的正常对照组(NC组),每组8只;28 d后ELISA法测定血浆PAI-1含量及活性,同时检测肺组织羟脯氨酸(HYP)含量。结果:NC组PAI-1含量(0.469 2±0.081 3)μg/L,活性(0.363 4±0.047 0)Au/ml,明显低于MD组和HD组(P<0.01);MD组PAI-1含量(8.920 5±1.094 8)μg/L,活性(2.066 7±0.598 6)Au/ml,高于HD组(3.479 8±0.487 2)μg/L、(1.225 3±0.199 4)Au/ml(P<0.01);NC组、HD组HYP低于MD组(P<0.01)。结论:水蛭可能通过减少凝血酶在肺内的表达,抑制PAI-1生成及活性,使重组尿激酶型纤溶酶原激活物(Urokinase plasmino-gen activator,uPA)活性升高,减少纤维蛋白沉积,对肺纤维化大鼠肺组织具有保护作用。
Objective： To investigate the effects of hirudo on the expression of plasminogen activator inhibitor-1（PAI-1） in rats with pulmonary fibrosis,and to explore the mechanisms.Methods： The pulmonary fibrosis rat model was established by intratracheal instillation of bleomycin.Model rats were divided into bleomycin group（group MD） and hirudo group（group HD） with 8 rats in each group,and control group（group NC） composed of 8 healthy rats was set up.The rats of group MD were given normal saline 6 ml/d by gavage.The rats of group HD were given hirudo power 4g/（kg·d） by gavage.Plasma PAI-1 level and its activity were detected by ELISA,and hydroxyproline（HYP） contents of lung tissues were detected.Results： The PAI-1 level and its activity in group NC were significantly lower than those in the other two groups（P0.01）.The PAI-1 level and its activity in group MD were higher than those in group HD（P0.01）.The HYP content in group NC and group HD were lower than that in MD group（P0.01）.Conclusions： Hirudo can protect the lung tissue of rats with bleomycin-induced pulmonary fibrosis by decreasing thrombin expression in the lungs,inhibiting PAI-1 generation and its activity,increasing urokinase plasminogen activator（uPA） activity and reducing the fibrous protein deposition.
出处
《贵阳医学院学报》
CAS
2012年第2期170-173,共4页
Journal of Guiyang Medical College
