目的　探讨金属基质蛋白酶 2 (MMP 2 )和金属基质蛋白酶抑制因子 2 (TIMP 2 )蛋白及mRNA在内毒素 (LPS)致新生大鼠肺损伤中的作用。　方法　将新生 7日龄大鼠 88只随机分为八组 ,即生理盐水对照组 (对照组 ) ,LPS注射后 30min组 ,1h ,2h ,4h ,8h组 (每组 8只 ) ,16h组 (16只 ) ,2 4h组 (2 4只 ) ,其中 16h组死亡 8只 ,2 4h组死亡 17只。观察不同时间点存活大鼠肺组织大体、光镜和电镜下的病理改变 ,应用免疫组化和RT PCR方法分别检测肺组织MMP 2和TIMP 2蛋白及mRNA的表达改变。　结果　病理改变证实了新生大鼠肺出血的发生 ,对照组MMP 2mRNA和蛋白的表达相对值分别为 (0 .5 2 3± 0 .0 30 )和 (12 6 .2 0± 17.98) ;注射LPS后 4h和 8hMMP 2mR NA(0 .82 6± 0 .5 6 7)和MMP 2蛋白 (15 0 .77± 9.80 )表达达高峰 ,差异有显著性 (P <0 .0 1)。TIMP 2蛋白及mRNA的表达无明显改变。　结论　用LPS制备了新生大鼠肺出血的动物模型 ,肺组织MMP 2的降解作用明显增加 ,可能导致肺出血的发生。 Objective To investigate the role of matrix metalloproteinase 2 (MMP 2) and matrix metalloproteinase 2 (TIMP 2) mRNA in lung injury induced by endotoxin (LPS) in neonatal rats. Methods Eighty-eight newborn 7-day-old rats were randomly divided into eight groups: normal saline group (control group), LPS injection 30min group, 1h, 2h, 4h and 8h groups 16), 24 hours group (24 rats), of which 8 died in 16h group and 17 died in 24 hours group. The pathological changes in the lung tissue, light and electron microscopy of the surviving rats at different time points were observed. The expressions of MMP 2 and TIMP 2 protein and mRNA were detected by immunohistochemistry and RT-PCR respectively. Results Pathological changes confirmed the occurrence of pulmonary hemorrhage in neonatal rats. The relative expressions of MMP-2 mRNA and protein in the control group were (0. 523 ± 0. 30) and (12 6 .2 ± 17. 98), respectively. After 4h and 8h, the expression of MMP2mRNA (0. 82 6 ± 0. 57 6 7) and MMP 2 protein (15 0 .77 ± 9.80) reached the peak, the difference was significant (P <0.01). TIMP 2 protein and mRNA expression did not change significantly. Conclusion The animal model of pulmonary hemorrhage in neonatal rats was prepared by LPS. The degradation of MMP 2 in lung tissue was significantly increased, which may lead to pulmonary hemorrhage.