Enhanced Expression of miR-34a Enhances Escherichia coli Lipopolysaccharide-Mediated Endometritis by Targeting LGR4 to Activate the NF-κB Pathway

Figure 4

LGR4 inhibits the inflammatory response by blocking NF-κB phosphorylation. Cells were transfected with 200 nM si-LGR4 or si-NC for 24 h and then treated with LPS (1.0 μg/ml) for 6 h. (a) The expression of LGR4 and phosphorylated NF-κB p65 in BENDs was determined by western blot. (b, c) The levels of LGR4 and phosphorylated NF-κB p65 were determined by IPP in BENDs. (d, e) Translocation of the p65 subunit from the cytoplasm into the nucleus was evaluated by immunofluorescence. Blue spots represent cell nuclei, and green spots represent p-p65 staining. Data are presented as the of three independent experiments (). versus the si-NC group; ^# versus the si-NC and LPS groups (cells transfected with si-NC after stimulation with LPS) (Student’s -test).

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