蛋白酶激活受体-1在肺纤维化大鼠肺组织中的表达

目的探讨在博莱霉素所致大鼠肺纤维化模型肺组织中蛋白酶激活受体-1的表达。方法将体重180-250g的SD清洁级雄性大鼠48只,按完全随机方法分为对照组及博莱霉素(BLM)组,BLM组大鼠气管内注入0.9-1.25ml博莱霉素A5(BLMA5,5mg/kg),对照组在同样条件下向气管内注入等量的生理盐水。两组动物于气管灌注后第7、14、28、40d分别随机处死6只。组化方法检测肺组织PAR-1的表达;Masson染色检测肺组织纤维化,按Ashcroft评分法,评估肺纤维化的严重程度,结果(1)对照组无明显胶原沉积,BLM组随着时间的延长,可见明显胶原沉积,BLM组/对照组两组在第7、14、28、40d肺间质纤维化Ashcroft评分分别为24±3.72/3±0.63、46.4±4.09/4±0.63、69.3±3.78/3±1.41、64.5±5.96/3±1.67,两组有显著性差异(P﹤0.05)。(2)BLM组/对照组两组在第7、14、28、40d平均每高倍镜视野肺组织PAR-1阳性细胞数分别为:9.93±1.47/2.5±1.52、16.67±2.16/1.83±1.17、17.67±2.16/2.17±0.75、16.0±2.28/2.17±1.17。BLM组各时间点肺组织PAR-1阳性细胞数较正常对照组增多,两组具有显著统计学差异(P﹤0.05)。(3)肺间质纤维化程度与PAR-1阳性细胞数呈正相关(r=0.76)。结论博莱霉素所致大鼠肺纤维化模型肺组织中蛋白酶激活受体-1的表达增强;蛋白酶激活受体-1的表达可能在博来霉素所致肺纤维化中其重要作用。

Expression of PAR-1 in the rat of bleonmycin-induced pulmonary fibrosis

Objective To explore the expression of PAR-1 in the lung in the in bleomycin-induced pulmonary fibrosis.Methods 48 Male SD rats were randomly divided into two groups：control group,model group.saline were instilled intratracheally in a dose of 5ml/kg in control group;Bleomycin A5 were instilled intratracheally in a dose of 5ml/kg inmodol group.6 Rats were sacrificed on 7d,14d,2d8,40din control/model group.Expression levels of PAR-1 in lung tissues were examined by immunohistochemistry.Results（1）In comparison with control group,collagen deposition were significant,Interstitial pulmonary fibrosis Ashcroft scores were 24±3.72、3±0.63,46.4±4.09、4±0.63,69.3±3.78,3±1.41,64.5±5.96,3±1.67,in model VS control group,respectively,on 7d,14d,28d,40d.（2）In comparison with control group,the expression of PAR-1 in lung tissue in model group were increased significantly.The cells of positive PAR-1 staining per high power lens were 9.93±1.47/2.5±1.52,16.67±2.16/1.83±1.17,17.67±2.16/2.17±0.75,16.0±2.28/2.17±1.17 in model VS control group,respectively,on 7d,14d,28d,40d.（3）Interstitial pulmonary fibrosis and PAR-1-positive cells was positively correlated（r=0.76）.Conclusion Expression of PAR-1 increased in the lung in the in bleomycin-induced pulmonary fibrosis.PAR-1 expression may play an important role in bleomycin-induced pulmonary fibrosis.