Pseudoprotodioscin (PPD), a phytoestrogen isolated from Dioscorea nipponica Makino, is recognized to possess anti-inflammatory and antiadipogenic capacities. PPD administration alleviated atherosclerotic lesions by lowering total cholesterol in ovariectomized apoE-/- mice fed a high-cholesterol diet. In Hep G2 cells, Pseudoprotodioscin increases ABCA1 protein and mRNA levels, and promotes the effluxion of ApoA-1-mediated cholesterol. Pseudoprotodioscin inhibits SREBP1c and SREBP2 transcription by decreasing microRNA 33a/b levels[3]. Pseudoprotodioscin, a furostanoside, inhibits SREBP1/2 and microRNA 33a/b levels and reduces the gene expression regarding the synthesis of cholesterol and triglycerides. Upon PPD treatment, ERα and endothelial nitric oxide synthase (eNOS) protein levels were increased, whereas cell adhesion molecule and monocyte chemoattractant protein-1 (MCP-1) mRNA levels were suppressed in human umbilical vein endothelial cells (HUVECs) after injury caused by oxidized low-density lipoprotein (ox-LDL)[4].
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