Conclusion
LncRNA-NEF regulated hyperoxia-caused inflammatory response, oxidative damage and apoptosis of RLE-6TN and MLE-12 cells by affecting the expression of FOXA2.
Material and methods
In this study, we used the lentivirus to establish the lncRNA-NEF overexpression RLE-6TN and MLE-12 cells. After that, the lentivirus was also used to knockdown the expression of FOXA2 in the two lncRNA-NEF overexpression cells. ELISA was performed to detect the levels of TNF-α, IL-1β and IL-6. The production of ROS, SOD, MDA and LDH was determined with the commercial kits. The apoptosis rates of these cells were measured with the flow cytometry.
Methods
In this study, we used the lentivirus to establish the lncRNA-NEF overexpression RLE-6TN and MLE-12 cells. After that, the lentivirus was also used to knockdown the expression of FOXA2 in the two lncRNA-NEF overexpression cells. ELISA was performed to detect the levels of TNF-α, IL-1β and IL-6. The production of ROS, SOD, MDA and LDH was determined with the commercial kits. The apoptosis rates of these cells were measured with the flow cytometry.
Results
The secretion of TNF-α, IL-1β and IL-6 was inhibited in RLE-6TN and MLE-12 cells after the overexpression of lncRNA-NEF. Furthermore, the production of ROS, MDA and LDH was also suppressed after the upregulation of lncRNA-NEF. The promotion of lncRNA-NEF also restricted the hyperoxia-induced apoptosis. However, the knockdown of FOXA2 abolished all the inhibitory effects exerted by lncRNA-NEF.