Formononetin Ameliorates LPS-Induced Endometrial Epithelial Cell Injury in Rats via TLR4/MyD88/NF-κB Signaling Pathway
Objective:To investigate the effect of formononetin on lipopolysaccharide(LPS)-induced endometrial epithelial cell injury in rats by regulating the Toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear transcription factor-KB(NF-κB)signaling pathway.Methods:LPS was used to establish the rat model of endometrial epithelial cell injury.The Cell Counting Kit-8(CCK8)assay was employed to examine the cell viability.TLR4 overexpression efficiency was detected by real-time PCR(RT-qPCR).Cell apoptosis was de-tected by flow cytometry.Enzyme-linked immunosorbent assay(ELISA)was employed to determine the levels of tumor necrosis factor-α(TNF-α),interleukin(IL)-1β,and IL-6.Western blotting was employed to determine the expression of TLR4/MyD88/NF-κB pathway-re-lated proteins.Results:Compared with the normal control group,the model control group showed increased cell inhibition rate and apoptosis rate,elevated levels of TNF-α,IL-1β,and IL-6,and up-regulated protein levels of p-p65/p65,p-IκBα/IKBα,MyD88,and TLR4(P＜0.05 or P＜0.01).Compared with the model control group,formononetin(12 μmol/L)decreased the cell inhibition rate and apoptosis rate,lowered the levels of TNF-α,IL-1β,and IL-6,and down-regulated the protein levels of p-p65/p65,p-IκBα/IκBα,MyD88,and TLR4(P＜0.05 or P＜0.01).Compared with the model+formononetin+Ov-NC group,the model+formononetin+Ov-TLR4 group demonstrated in-creased cell inhibition rate and apoptosis rate,risen levels of TNF-α,IL-1β,and IL-6,and up-regulated protein levels of p-p65/p65,p-IKBα/IKBα,MyD88,and TLR4(P＜0.05 or P＜0.01).Conclusion:Formononetin can down-regulate the expression of TLR4 to inhibit the activation of TLR4/MyD88/NF-κB signaling pathway,thereby reducing LPS-induced apoptosis and ameliorating inflammatory injury of endo-metrial epithelial cells in rats.
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