A novel cross-linkable, high molecular weight poly(diisoamyl itaconate-co-isoprene) (PDII) elastomer was prepared by emulsion polymerization based on itaconic acid, isoamyl alcohol, and isoprene. Both persulfate and redox initiators were used for the copolymerization of diisoamyl itaconate and isoprene at different monomer ratios. Redoxinitiated PDII has much higher molecular weight but relatively lower yield than the persulfate-initiated one. PDII with a number-average molecular weight of 352 000 and a glass transition temperature of −39.5 °C was obtained when the mass ratio of diisoamyl itaconate to isoprene was 80/20. Diisoamyl itaconate and isoprene reactivity ratios were determined by two conventional linear methods: the Fineman−Ross method and the Kelen−Tudos method. Molecular dynamics simulation and FTIR were used to study the interaction between silica and PDII macromolecules, and the result showed that hydrogen bonds were formed between silica silanols and PDII macromolecules. Silica-reinforced PDII exhibited good mechanical performance, such as ultimate tensile strength above 11 MPa and elongation at break above 400%.

Diosgenyl saponins are the most abundant steroid saponins, and exert a large variety of biological functions. In a previous report, we showed that dioscin was able to induce cytotoxicity and apoptosis in human myeloblast leukemia HL-60 cells. This study further investigated the action mechanisms underlying this effect. The activation of caspase-9 and -3, but not caspase-8, together with the down-regulation of anti-apoptotic Bcl-2 protein, demonstrated that the apoptotic signaling triggered by dioscin was mediated through the intrinsic mitochondriadependent pathway. We also investigated its anti-proliferative effect on human chronic myelogenous leukemia K562 cells. Flow cytometry analysis showed that dioscin treatment induced the accumulation of cells in the G 2 /M phase. Cytomorphology with DAPI and Wright-Giemsa staining demonstrated the enlargement of cell volume and multinucleation in the treated cells. Subsequent apoptosis was delineated with phosphatidylserine externalization and DNA hypodiploidy. Trillin was one of the hydrolysates of dioscin. We demonstrated that it could induce multinucleation in HL-60, K562 and human promyelocytic leukemia NB 4 cells, suggesting its extensive mitotic-arresting effects. As the diosgenyl sapogenin, diosgenin was also shown to be able to induce multinucleation and apoptosis in K562 cells in a similar manner to dioscin. These findings suggest that diosgenyl saponins have the properties to induce mitotic arrest and apoptosis, suggesting that they may be a new kind of antimitotic agent.

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