内毒素诱导大鼠急性肺损伤中凋亡相关基因bcl-2及fas的表达观察

Studies on the expression bcl-2 and fas in acute lung injury induced by lipopolysaccharide in rats

【目的】探讨bcl-2及fas在内毒素诱导大鼠急性肺损伤(ALI)中的表达。【方法】Wistar大鼠随机分为正常对照组及脂多糖(LPS)股静注后30、60、120 min组,检测肺损伤指标(肺系数、PMN百分比、蛋白含量、肺泡通透指数)、观察病理形态、免疫组化染色检查。【结果】表征损伤的各生化指标对照组均较损伤组轻;其中LPS 120 min变化组最为显著,各项生化指标均较对照组明显升高(P<0.001);肺组织各蛋白LPS致伤后较正常组表达增高(P<0.01)。【结论】Bcl-2和fas系统参与了LPS致ALI时的肺损伤,并在ALI发病机制中起着一定的作用。

[Objective] To study the expression of apoptosis related gene bcl-2 and fas in acute lung injury （ALI） of rat. [ Method] ALI animal model was prepared by fermoral vein injection of lipopolysaccharide （LPS） at different time intervals. Lung injury index （lung coeficent, leucocyte number in BALF, neutrophil percentage, protein content and pulmonary alveolus index） and pothological changes at different time intervals were compared. [Results] In LPS 2 h group the lung injury index and pathological changes altered significantly. The results of IHC showed that the positive expression of bcl-2 and fas in lung constitution were higher than that in control （ P 〈 0.01）. [Conclusion] By clearing free radical Bcl-2 and fas could induce the expression of bcl-2, and inhibit the expression of fas gene, and finally prevent the process of apoptosis.