Phosphorylation of p38MAPK in hyperoxia-induced lung injury of new-born rats
Liman Luo
Abstract
Liman Luo
Abstract
Objective To investigate the expression and significance of p38 mitogen-activated protein kinase (p38MAPK) in hyperoxia-induced lung injury of new-born rats. Methods Totally 160 rats at the age of 12 h were randomly and equally divided into air control group, hyperoxia-induced lung injury group, hyperoxia-induced lung injury+SB203580 group and hyperoxia-induced lung injury + normal saline group. After the injury was inflicted, SB203580 or normal saline at same volume was given intraperitoneally at 5 mg/kg. After the rats were executed at the time points of 12, 24, 72 h and 1 week after the model establishment, the right upper lungs were resected for histopathology, right below lungs for wet weight/dry weight, and left lungs for detecting the expression of p38MAPK by Western blot analysis. Results Hyperoxia-induced lung injury model were established successfully after 72 h by exposure to hyperoxia. No p38MAPK expression was observed in air control group. In hyperoxia-induced lung injury group p38MAPK was detected from 12 h, reached to the peak at 72 h, and decreased 1 week later, and its expression was significantly higher in this group and normal saline group than in SB203580 group. Conclusion p38MAPK is involved in the process of hyperoxia-induced lung injury, and the injury can be relieved by treatment of SB203580.
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Objective To investigate the expression and significance of p38 mitogen-activated protein kinase (p38MAPK) in hyperoxia-induced lung injury of new-born rats. Methods Totally 160 rats at the age of 12 h were randomly and equally divided into air control group, hyperoxia-induced lung injury group, hyperoxia-induced lung injury+SB203580 group and hyperoxia-induced lung injury + normal saline group. After the injury was inflicted, SB203580 or normal saline at same volume was given intraperitoneally at 5 mg/kg. After the rats were executed at the time points of 12, 24, 72 h and 1 week after the model establishment, the right upper lungs were resected for histopathology, right below lungs for wet weight/dry weight, and left lungs for detecting the expression of p38MAPK by Western blot analysis. Results Hyperoxia-induced lung injury model were established successfully after 72 h by exposure to hyperoxia. No p38MAPK expression was observed in air control group. In hyperoxia-induced lung injury group p38MAPK was detected from 12 h, reached to the peak at 72 h, and decreased 1 week later, and its expression was significantly higher in this group and normal saline group than in SB203580 group. Conclusion p38MAPK is involved in the process of hyperoxia-induced lung injury, and the injury can be relieved by treatment of SB203580.
Key concepts: Hyperoxia, Lung, Saline, Western blot, Medicine, Anesthesia, Andrology, Pathology