目的：探讨肿瘤坏死因子α(TNFα)及半胱氨酸蛋FB白酶3(Caspase3)在早产大鼠高氧肺损伤中的动态表达及其意义。方法：孕21d的SD早产大鼠生后第2天,随机分为空气组和高氧组(均n=40)。高氧组大鼠予以85%高氧持续暴露,空气组大鼠置于空气中。于高氧暴露1d、4d、7d、14d和21d每组各处死8只大鼠,收集肺组织标本,苏木精-伊红染色观察肺组织病理形态学变化,双抗夹心ELISA法检测TNFα含量,免疫组化和Westernblot检测Caspase3表达。结果：高氧暴露4d、7d和14d肺组织TNFα和Caspase3含量明显增高(均P<0.01),且两者之间具有显著相关性(r=0.93,P<0.01)。结论：TNFα诱导Caspase3过度表达导致细胞凋亡可能是早产大鼠高氧肺损伤的发病机制之一。

OBJECTIVE: To explore the temporal expression of tumor necrosis factor-α(TNF-α) and Caspase-3 in hyperoxia-induced lung injury in preterm rats. METHODS: Two-day-old Sprague-Dawley preterm rats were randomly divided into Air group and Hyperoxia group (both n=40). Rats in the Hyperoxia group were exposed to 85% O_2, while rats in the Air group were exposed to air. The rats in each group were sacrificed at 1, 4, 7, 14 and 21 days after exposure (8 rats at each time point), and lung tissues were collected. Pathomorphology of the lungs was observed by hematoxylin-eosin staining. The contents of TNF-α in the homogenate of lungs were detected using ELISA. The expression of Caspase-3 was detected by immunohistochemistry and Western blot. RESULTS: The contents of TNF-α in the homogenate of lungs increased significantly at 4, 7 and 14 days after exposure, and the expressions of Caspase-3 were also enhanced, as compared with those of the Air group(P<0.01). The expression of Caspase-3 positively correlated with the contents of TNF-α (r=0.93,P<0.01). CONCLUSIONS: Over-expression of Caspase-3 induced by TNF-α might be one of the underlying mechanisms of hyperoxia-induced lung injury in preterm rats