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[目的]探讨胰岛素样生长因子-1(IGF-1)对高氧性肺损伤的保护作用及其机制.[方法]选择Wistar新生大鼠,建立高氧模型后分为空气组、高氧组(85%体积分数的氧)及治疗组(85%体积分数的氧+IGF-1),治疗组腹腔注射给予IGF-1.采用核染色结合TUNE法观察各组肺细胞凋亡情况,利用Western blot法检测各组肺组织中c-Jun氨基末端激酶(JNK)、p-JNK及CCAAT增强子结合蛋白同源蛋白(CHOP)表达水平.[结果]高氧组高氧3,7,14d时肺细胞凋亡指数较同一天空气组明显增高(P<0.05),治疗组3,7,14d时肺细胞凋亡指数较同一天高氧组明显降低(P<0.05).高氧组3,7,14d时JNK,p-JNK,CHOP蛋白含量与空气组比较明显增高(P<0.05),而治疗组上述蛋白含量与同一天高氧组比较明显降低(P<0.05).[结论]IGF-1对高氧肺损伤的保护作用与下调ERS相关的JNK,p-JNK,CHOP蛋白表达水平有关系,提示IGF-1通过ERS及UPR信号途径对高氧性肺损伤起保护作用.
[Objective] To explore the protective effect and mechanism of insulin-like growth factor-1 (IGF-1) on lung injury induced by hyperoxia.Methods Wistar neonatal rats were selected to establish hyperoxia model and then divided into air group, hyperoxia group (85% volume fraction of oxygen) and treatment group (85% volume fraction of oxygen + IGF-1) were given intraperitoneal injection of IGF-1.The nuclear staining and TUNE method were used to observe the apoptosis of lung cells in each group. blot was used to detect the expression of c-Jun N-terminal kinase (JNK), p-JNK and CCAAT enhancer binding protein homology protein (CHOP) in lung tissue of each group. [Results] The apoptosis index of lung cells in the hyperoxia group was significantly higher than that in the same day (P <0.05), and the apoptosis index of lung cells in the treatment group at 3, The levels of JNK, p-JNK and CHOP protein in the treatment group were significantly lower than those in the air group at 7 and 14 days (P <0.05), while those in the treatment group were significantly lower than those in the hyperoxia group on the same day (P <0.05). [Conclusion] 1 on the hyperoxia-induced lung injury and down-regulation of ERS-related JNK, p-JNK, CHOP protein expression, suggesting that IGF-1 through the ERS and UPR signaling pathways for the protection of hyperoxia lung injury .