血必净对脂多糖诱导的急性肺损伤大鼠肺组织纤溶酶原激活物抑制剂-1表达的影响

目的观察脂多糖诱导的急性肺损伤(ALI)大鼠PAI-1的表达及血必净的干预效果,并探讨作用机制。方法 45只Wistar大鼠随机分为三组:(1)健康对照(Control)组(15只)、(2)脂多糖(LPS)组(15只)、(3)血必净干预(XBJ)组(15只)。LPS组和XBJ组采用股静脉注射LPS(5 mg/kg)建立大鼠ALI模型。造模前半小时开始给药,XBJ组给予血必净4 ml/kg,iv;Control组和LPS组则给予等容积0.9%氯化钠注射溶液。在造模后6 h、12 h、24 h各随机处死大鼠5只,分别作为Ⅰ、Ⅱ、Ⅲ亚组,光镜下观察肺脏组织形态学变化,免疫组织化学法(IHC)检测肺组织中PAI-1蛋白表达。结果造模后,LPS组随着实验时间的延长,肺组织PAI-1蛋白呈逐渐增加趋势,至12 h达到高峰。与LPS组相比,血必净组各时间点肺组织PAI-1蛋白表达明显降低(P<0.05)。光镜显示LPS组肺组织病理形态学改变明显,而血必净组则明显减轻。结论血必净可抑制脂多糖诱导的急性肺损伤大鼠肺组织增强的PAI-1表达,减轻脂多糖诱导的大鼠肺损伤程度。

The effect of Xuebijing on expression of PAI-1 in lipopolysaccharide-induced acute lung injury in rats

Objective To study plasminogenactivator inhibitor-1（PAI-1）expression in lipopolysaccharide-induced acute lung injury in rats and investigate the effect of Xuebijing and the possible mechanisms.Methods 45 Wistar rats were randomly divided into 3 groups as following：（1）control group（n=15）,（2）LPS group（n=15）,（3）Xuebijing treatment group（XBJ group）（n=15）.LPS（5mg/kg）was infused by femoral vein to reproduce ALI model in LPS group and XBJ group.Male Wistar rats were given either saline（LPS group）or XBJ（XBJ＋LPS group）4ml/kg 30 min before the intravenous injection of a bolus of LPS,whereas control group were given equivalent volume normal saline.Five rats in each group were killed at 6h,12h and 24h,which were divided into subgroupI,Ⅱ,Ⅲ,and 1ung tissue was collected.The pathomorphism changes of lung tissue were observed using light microscope,and pulmonary PAI-1 protein expression was examined by immunohistochemistry in all rats.Results Lung tissue PAI-1 protein expression showed a gradual increase and reached the peak at 12h in LPS group after establishing model.Lower levels of PAI-1 protein were found in Xuebijing group than that in LPS group at all time points（P0.05）.The pathological change was obvious in LPS group,which was more severe than XBJ group under microscope.Conclusion Xuebijing could attenuate the degree of acute lung injury in rats induced by LPS,which may be related to its effect in inhibiting the increased PAI-I protein expression of lung tissue.