Objective To explore the effect of DFMG on the inflammatory injury of human umbilical vein endothelial cells (HUVE-12) induced by LPC and its possible mechanism.Methods HUVE-12 was deal with different concentrations of LPC and the appropriate concentration of LPC was chosen to prepare cell inflammatory injury model. HUVE-12 cells were pretreated with DFMG or a specific antagonist of TLR4 (CLI-095) then deal with optimal concentration of LPC, the proliferation of HUVE-12 was detected by MTT, the expression level of TNF-α and LDH in the culture was detected by ELISA and the expression of TLR4 /MyD88 protein were measured western blot.Results LPC inhibited the proliferation of HUVE-12 cells and promoted the secretion of TNF-α, the release of LDH and expression of TLR4, MyD88 protein. DFMG inhibited the effect of LPC on the proliferation of HUVE-12, the secretion of TNF-α, the release of LDH and expression of TLR4/MyD88 protein in dose-dependent manner.Conclusion DFMG may play an important role in protecting endothelial cells from inflammatory injury induced by LPC. The mechanism of DFMG on protecting endothelial cells from oxidative injury in HUVEC-12 cells maybe probably associate with inhibiting the TLR4-MyD88 signal transduction.

Objective To study the effect and mechanism of fructus viticis total flavonoids(FVTF) on the migration and invasion ability of SMMC-7721-derived liver cancer stem-like cells(LCSLCs). Methods The second generation of sphere forming cells(SFCs) obtained from SMMC-7721 cell line using suspension culture with the stem cell conditioned medium were used as LCSLCs. LCSLCs were treated with 0.1% DMSO or different concentrations of FVTF. The effects of FVTF on migration and invasion of LCSLCs was determined using cell migration assay and transwell invasion assay. The mechanism of FVTF action was explored by analyzing the level of FoxM1 and MMP2 protein expression with Western bolt. Results Compared with the control group,FVTF could downregulate the expression of FoxM1 and MMP2 protein and significantly inhibited the migration and invasion of LCSLCs in a concentration dependent manner. Conclusion FVTF effectively inhibited the migration and invasion ability of SMMC-7721-derived LCSLCs is associated with blockage of FoxM1–MM P2 signal axis.