Effect of L-Se-methylselenocysteine on expression of inflammatory fac-tors in THP-1 cell-derived foam cells and its mechanism
AIM:To investigate the mechanism by which L-Se-methylselenocysteine(L-SeMSC)inhibits foam cell formation in THP-1-derived macrophages from human monocytic leukemia cells.METHODS:THP-1-derived macrophages were first induced using phorbol 12-myristate 13-acetate(PMA),followed by the use of oxidized low-density lipoprotein(ox-LDL)to establish a foam cell model.The effects of various concentrations of L-SeMSC on THP-1 cell via-bility and apoptosis were assessed using the CCK-8 assay and flow cytometry.Lipid droplet accumulation was visualized through oil red O staining.Additionally,the mRNA levels of interleukin-1β(IL-1β),intercellular adhesion molecule 1(ICAM-1),fatty acid translocase(FAT/CD36),solute carrier family 27 member 4(SLC27A4),and superoxide dis-mutase 1(SOD1)were measured using qRT-PCR.The levels of inflammatory proteins,including IL-6,IL-1β,tumor ne-crosis factor-α(TNF-α),matrix metalloproteinase 9(MMP9),and nuclear factor-κB(NF-κB)signaling-related proteins in activated B cells were assessed via Western blot.RESULTS:Treatment with L-SeMSC at concentrations ranging from 25 to 200 µmol/L enhanced cell viability,with no significant impact on apoptosis observed across the different concentra-tions.The accumulation of lipid droplets was notably reduced in the L-SeMSC group compared to the ox-LDL group.The mRNA levels of lipid transport-related genes(CD36 and SLC27A4)and inflammation-related genes(IL-1β and ICAM-1)were significantly decreased,while SOD1 mRNA levels increased significantly.Furthermore,the expression levels of in-flammatory proteins IL-1β,IL-6,TNF-α,MMP9,and phosphorylated p65(p-p65)were markedly reduced.CONCLU-SION:L-SeMSC may exert anti-atherosclerotic effects by decreasing inflammatory factor levels,inhibiting foam cell for-mation,and reducing lipid droplet accumulation in macrophages.The associated anti-inflammatory mechanism appears to primarily involve the modulation of key proteins in the NF-κB signaling pathway.
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