Differentiation of preadipocytes into adipocytes is a major step leading to obesity. This study examines the effects of isorhamnetin, a metabolite of quercetin, at physiological and supraphysiological concentrations on the differentiation of 3T3-L1 pre-adipocyte to adipocyte. Comparison was made with the effect of quercetin on 3T3-L1 differentiation under the same conditions. Cell viability during adipocyte differentiation for 8 days in the presence of isorhamnetin and quercetin was above 94 and 97%, respectively. Oil Red O staining showed significant differences (P < 0.05) between the effect of isorhamnetin or quercetin on cytoplasmic lipid droplet accumulation and control untreated cells. Isorhamnetin at physiologically attainable concentrations was more effective than quercetin in inhibiting cytoplasmic lipid droplet accumulation. Neither isorhamnetin nor quercetin had an effect on the expression of macrophage chemoattractant protein-1 (MCP-1). CCAAT/enhancer binding protein α (C/EBP-α) was down-regulated by isorhamnetin. Compared to the control, isorhamnetin or quercetin decreased PPAR-γ 1 and 2 expressions. The data indicate that isorhamnetin was more effective than quercetin at physiologically attainable concentrations in reducing lipid accumulation in 3T3-L1 pre-adipocytes.

Hypoxia-inducible factor -1 alpha (HIF-1α), vascular endothelial growth factor (VEGF), and phosphorylated Akt (p-Akt) are critical in pancreatic cancer cell growth, angiogenesis and metastasis. The ability of MIA Paca-2 pancreatic cancer cells to migrate and invade after treatment with juglone (5 hydroxy-1, 4-naphthoquinone) was analyzed by a transwell invasion and migration assay, a wound healing assay, and an in vitro tube formation assay using human umbilical vein endothelial cells (HUVEC). ELISA was used to determine the levels of HIF1-α. Western blot analysis was used to determine the level of VEGF, p-Akt, and carbonic anhydrase IX expression. Juglone down-regulated the expression of HIF-1α, VEGF, and significantly suppressed the phosphorylation of Akt. Juglone dose-dependently inhibited the metastatic potential of pancreatic cancer cells by inhibiting cell migration, invasion and wound healing assays. Juglone attenuated the aggressiveness of pancreatic cancer cells in vitro.