[Temporal expression and significance of caspase-3 and interleukin-8 in the lungs of preterm rats exposed to hyperoxia].

OBJECTIVE: To explore the temporal expression and significance of Caspase-3 and interleukin-8 (IL-8) 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 (each rats in each group). 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 lungs was observed by hematoxylin-eosine staining. The contents of IL-8 in the homogenate of lungs were detected using ELISA. The expression of Caspase-3 was detected by immunohistochemistry and Western blot. RESULTS: (1) Lung histopathology: after hyperoxia exposure 1 day, no significant effects on alveoli were found; but on days 4 and 7, alveolitis appeared: there were necrotic abscission cells in alveolar space, increased inflammatory cells infiltration, lung interstitial edema; on days 14 and 21, lung structure derangement, decreased number of alveoli, simplified and vesicular lung structure, all of which showed the retardation of alveolar formation. (2) the contents of IL-8 in the homogenate of lungs had no significant change on day 1 but increased significantly on days 4, 7 and 14 compared with air control group (P < 0.01 for all). (3) Immunohistochemistry detected the expression of Caspase-3 in the lung: the intensity of Caspase-3 expression increased significantly on days 4, 7 and 14 compared with air control group (P < 0.01). (4) Western blotting detected the expression of caspase-3 in the lung: the pattern of dynamic expression of Caspase-3 was similar to the results of immunohistochemistry. CONCLUSIONS: Both apoptosis and necrosis contribute to cell death during hyperoxia. Apoptosis and necrosis may both play an important role in hyperoxia-induced lung injury in preterm rats.