ABSTRACT
OBJECTIVE:To prepare Idebenone solid dispersion,and to investigate its dissolution rate in vitro. METHODS:Us-ing Poloxamer 407(P407)as carrier,the influence of preparation methods(solvent method,melting method)and the ratio of the drug to P407(1∶1,1∶3,1∶8)on the dissolution of drug were investigated by single factor design. The state of idebenone in ma-trix of solid dispersion was further determined by using differential scanning calorimetry (DSC) and X-ray powder diffraction (XRD). RESULTS:Idebenone solid dispersion prepared by solvent method(the ratio of the drug to poloxamer was 1∶3)showed dissolution rate of 80%. The majority of idebenone existed in the solid dispersion at amorphous forms or molecular state. CONCLU-SIONS:Idebenone solid dispersions with high dissolution rate in vitro is prepared successfully.
ABSTRACT
Objective: To study the effect of sulforaphane (SUL) on cell growth inhibition, cell cycle, apoptosis and its mechanism in different breast cancer cell lines. Methods: By means of MTT assay, flow cytometry and Western blotting, the effects of the SUL different concentrations on cell growth inhibition, cell cycle arrest, F3Ⅱapoptosis and expression of p34cdc2 and Cdc25C were studied. Results: (1) SUL had strong inhibition effects on the cell growth of tested mammary cancer cell lines, in which the sensitivity of ERP cell lines to SUL was stronger than that of ERN cell line. (2) SUL exhibited obviously G2/M cell cycle arrest to F3Ⅱ and two kinds of ERP cell lines at 5-10?mol/L, whereas no effect on the cell cycle of ERN cell line. (3)The mechanism of hindering transition of F3 Ⅱ cells from G2 phase to M phase was enhancing the phosphorylation of Cdc2, down-regulating the expression of Cdc25C, and inducing inhibition to thedephosphorylation of cyclin B1-Cdc2 complex. (4) No apoptosis was observed under tested conditions. Conclusion: Sulforaphane exhibited obvious differences in the inhibiting effects on the cell proliferation and cell cycle arrests of four different tested breast cancer cell lines, and did not induce apoptosis in F3Ⅱcell line under tested conditions. The mechanism of cell cycle arrest of F3Ⅱcell line appears to involve enhancing the phosphorylation of Cdc2, and down-regulating the expression of Cdc25C.
ABSTRACT
Objective: The effects of purple-fleshed sweet potato anthocyanin (PSA) on anti-oxidation and anti-aging were investigated. Methods: The effects of different doses of PSA(100、 500、1000 mg/kg bw)on the serum T-AOC were investigated in aged mice after administration for 3 d, 10 d and 18 d. The content of MDA, the activity of serum SOD and blood GSH-Px were measured, and compared with those in Vit E and control group after 30 d. Result: PSA significantly increased the serum T-AOC in aged mice, and this increment was higher when given longer. PSA significantly decreased MDA and enhanced SOD and GSH-Px activities. The efficiency on antioxidative capacity of aged mice at PSA 100 mg/kg bw was equivalent to that of vitamin E at the same amount (100 mg/kg bw). The antioxidation state of 13 mo mice given PSA at 1000 mg/kg bw was near to that of 4 mo mice. Conclusion: PSA has marked effect of antioxidation and can delay aging.