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Dioscin suppressed HL-60 cell growth in a dose-dependent manner. Dioscin induces apoptosis by activation of p38 MAPK and JNK through the caspase-dependent mitochondrial death pathway. Dioscin may be used as a compound lead for the treatment of myeloblast leukemia. Dioscin may be a potential anticancer drug, which efficiently inhibits angiogenesis induced by VEGFR2 signaling pathway as well as AKT/MAPK pathways. Dioscin alleviated body weight and liver lipid accumulation symptoms, increased oxygen consumption and energy expenditure, and improved the levels of serum and hepatic biochemical parameters. Dioscin significantly attenuated oxidative damage, suppressed inflammation, inhibited triglyceride and cholesterol synthesis, promoted fatty acid β-oxidation, down-regulated MAPK phosphorylation levels, and induced autophagy to alleviate fatty liver conditions. Dioscin prevents diet induced obesity and NAFLD by increasing energy expenditure.
| Molecular Weight | 869.04 |
| Formula | C45H72O16 |
| CAS Number | 19057-60-4 |
| Solubility (25°C) | DMSO 90 mg/mL |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
[1] Liu M, et al. Sci Rep. Potent effects of dioscin against obesity in mice.
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