Reactive oxygen species induce injury of the intestinal epithelium during hyperoxia

被引:45
作者
Zhao, Min [1 ]
Tang, Shimiao [1 ]
Xin, Junchi [1 ]
Wei, Yingliang [2 ]
Liu, Dongyan [1 ]
机构
[1] China Med Univ, Shengjing Hosp, Med Res Ctr, 36 Sanhao St, Shenyang 110000, Liaoning, Peoples R China
[2] China Med Univ, Shengjing Hosp, Dept Orthopaed Surg, Shenyang 110000, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
hyperoxia; reactive oxygen species; hydrogen peroxide; nuclear factor-B; apoptosis signal-regulating kinase 1; tumor necrosis factor-; hypoxia-inducible factor-1; NF-KAPPA-B; IMMUNOGLOBULIN-A; NEONATAL-RATS; SIGNALING PATHWAYS; BARRIER DEFENSE; LUNG INJURY; TNF-ALPHA; CELLS; APOPTOSIS; INFLAMMATION;
D O I
10.3892/ijmm.2017.3247
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Long-term therapeutic hyperoxia may exert serious toxic effects on intestinal epithelial cells in vitro and in vivo. The aim of the present study was to investigate the cause of this intestinal injury under conditions of hyperoxia. Caco-2 cells were treated with different concentrations of hydrogen peroxide (H2O2) and 85% hyperoxia for 24 h. Higher rates of injury of Caco-2 cells were observed in the hyperoxia and H2O2 groups compared with the control group. The reactive oxygen species (ROS) level of the hyperoxia group was significantly higher compared with that of the 400 M H2O2 group. The protein and gene levels of RelA, RelB, hypoxia-inducible factor-1, tumor necrosis factor- and apoptosis signal-regulating kinase 1 were significantly higher in the hyperoxia and H2O2 groups compared with those in the control group. In conclusion, during hyperoxia, intestinal epithelial cells were destroyed and the levels of ROS were increased. Therefore, ROS may play an important role in intestinal injury in a hyperoxic environment.
引用
收藏
页码:322 / 330
页数:9
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