关键词: 关键词：神经肽P物质, 高氧, 肺损伤, MAPKs

Abstract: Objective: To explore the impact of exposure to hyperoxia on lung tissue from premature rats. Meanwhile, rats were treated with substance P to observe whether it has an influence on hyperoxia-induced lung injury and MAPKs signaling pathway. Methods: Sixty premature Wistar rats were divided randomly into 4 groups: normoxic group， normoxic+SP group，hyperoxic group， hyperoxic+SP group. Each group was divided into 3 subgroups according to the 3 time points of 3d, 7d and 14d. Lung pathology was examined with light microscopy. Wet/dry (W/D) ratio of lung tissue, the content of SP in lung were evaluated. MDA, SOD and GSH-Px were detected. Cell apoptosis was detected by TUNEL. MAPKs was detected by Western blot. Results: The rats in hyperoxia groups had lung injury, and it was increased dependently with the time of exposure to hyperoxia, while treated with substance P the injury could be improved.The W/D ratio of rats in hyperoxia group was significantly increased(P＜0.05), while treated with substance P W/D ratio become reducing(P＜0.05). The content of SP in hyperoxia group was reduced and the content of SP was decreased dependently with the time of exposure to hyperoxia(P＜0.05). The vitality of MDA in the hyperoxia group was increased significantly, and the vitality of hyperoxia+SP group was decreased as compared with that in the hyperoxia(P＜0.05). The vitality of SOD,GSH-Px in the hyperoxia group was decreased(P＜0.05), which become much lower dependently with the time of exposure to hyperoxia, the vitality of SOD,GSH-Px were increased after treated with substance P(P＜0.05). TUNEL-positive cell of hyperoxia groups significantly increased inversely. TUNEL-positive cell was decreased as rats were treated with substance P. The results of Western blotting revealed that the expression of p-JNK,P38 and ERK protein was higher in the hyperoxia group than that in the normoxic group(P＜0.05)，and the expression of p-JNK,P38 and ERK protein increased in time dependently. However, the expression of p-JNK and P38 protein was lessened in hyperoxia+SP group(P＜0.05). The expression of ERK protein was increased in hyperoxia+SP group(P＜0.05). Conclusion: Hyperoxia can lead to lung injury in premature rats and treatment with SP could protect lung injury in oxidative stress condition by inhibiting MAPKs pathway.

Key words: Key Words: substance P , hyperoxia , lung injury , MAPKs