Propofol rescues LPS-induced toxicity in HRT-8/SVneo cells via miR-216a-5p/TLR4 axis.

OBJECTIVE: The purpose of this study was to evaluate the effect of propofol on lipopolysaccharide (LPS)-induced toxicity in HTR-8/SVneo cells. METHODS: In this study, HTR-8/SVneo cells were induced by LPS. The cells were treated with different concentrations of propofol. Cell proliferation, apoptosis, invasion, and wound healing rate were measured by MTT, flow cytometry, Transwell, and wound-healing assay. The relative mRNA expression levels of miR-216a-5p, TLR, MyD88, and NF-κB(p65) were measured by qRT-PCR. The protein expression levels of TLR, MyD88, and p-NF-κB(p65) were detected by western blot. The p-NF-κB(p65) nuclear volume was evaluated by cell immunofluorescence. RESULTS: Compared with control group, the cell proliferation, invasion, and wound healing rate were significantly decreased and the cell apoptosis rate was significantly increased in LPS- induced HTR-8/SVneo cells (P < 0.01). With propofol supplement, the cell proliferation, migration, and invasion abilities were significantly recovered and apoptosis rate was significantly inhibited (P < 0.05). The expression levels of miR-216a-5p, TLR4, MyD88, NF-κB(p65), and p-NF-κB(p65), and p-NF-κB(p65) nuclear volume were significantly different between propofol group and model group (P < 0.05). However, after knockdown of miR-216a-5p expression by si-miR-216a-5p transfection, the cell proliferation, migration, and invasion abilities were significantly inhibited and apoptosis rate was notably increased (P < 0.05). CONCLUSION: Propofol improves LPS-induced toxicity in HTR-8/SVneo cells via regulation miR-216a-5p/TLR4 axis.