LincRNA Cox-2 Regulates Lipopolysaccharide-Induced Inflammatory Response of Human Peritoneal Mesothelial Cells via Modulating miR-21/NF-κB Axis

Figure 4

The negative regulation between miR-21and TLR4, and the regulatory mechanism of Cox-2 in LPS induced HPMCs injury via NF-κB axis. (a) Target prediction of the binding sites between miR-21 and TLR4. Luciferase report of the luciferase activity between miR-21 and TLR4. (b) The expression of TLR4 after transfection with overexpressed and suppressive miR-21. (c) The TLR4 expression after transfection with si-RNAs. (d) MTT assay showed cell viability after different treatments. (e) Flow cytometry showed cell apoptosis after different treatments. (f) The concentration of inflammatory factors in supernatant of HPMCs after different transfections. (g) The expression of apoptosis-associated proteins after different transfections. (h) The expression of downstream genes of NF-κB axis after different treatments. (i) NF-κB nuclear translocation in HPMCs after different treatments by Flow cytometry. (j) The nuclear translocation ratio of NF-κB. The experiments were repeated in triplicate. Significance: and versus the controls.

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