Intrauterine Perfusion Of Prp Improves The Inflammatory Response Of Endometritis In Rats Through Mir-19a And Nf-Kb Pathway

Objective: To investigate the potential mechanism of PRP intrauterine infusion in treating inflammatory response of endometritis. Method: SD female rats were selected and randomly divided into control group (CG), model group (MG), PRP group, PRP+NC inhibitor group and PRP+miR-19a inhibitor group. In the MG, PRP group, PRP+NC inhibitor group and PRP+miR-19a inhibitor group, rats were all inoculated with Escherichia coli.Methods: In the PRP group, PRP+NC inhibitor group and PRP+miR-19a inhibitor group, rats received PRP intrauterine infusion. In the PRP+NC inhibitor group, rats were injected with NC inhibitor via tail vein after PRP treatment. In the PRP+miR-19a inhibitor group, rats were injected with miR-19a inhibitor via tail vein after PRP treatment. The levels of serum inflammatory factors, MDA and SDO were recorded in each group. The pathological changes of endometritis were detected by HE staining. The NF-kB protein was detected by Western blot. The miR-19a was detected by qPCR.Results: Endometritis caused an increase in serum phosphorylation levels of TNF-, IL-1, MCP, IL-10 and NF-kB protein, and a decrease in MDA, SOD and miR-19a. Endometritis resulted in degeneration and necrosis of endometrial epithelial cells, infiltration of scattered or lamellar inflammatory cells, and congestion and edema of endometrium. Intrauterine perfusion of PRP inhibited the phosphorylation levels of serum TNF-alpha, IL-1 beta, MCP, IL-10 and NF-kB protein, and increased MDA, SOD and miR-19a. Down-regulation of miR-19a could counteract the therapeutic effect of PRP on endometritis.Conclusion: Intrauterine perfusion of PRP could improve the inflammatory response of endometritis in rats through miR-19a and NF-kB pathway.