ABSTRACT
Objective: To investigate the chemical constituents from the stems of Syringa pinnatifolia. Methods: The chemical constituents were isolated and identified by chromatography on silica gel, ODS, and Sephadex LH-20 columns, as well as RP-HPLC. Their structures were elucidated on the basis of physicochemical properties and spectral analyses. Results: Eleven compounds were isolated from S. pinnatifolia and their structures were identified as secoisolariciresinol (1), (8R, 8'R, 9R)-4, 4'-dihydroxy-3, 3', 9-trimethoxy-9, 9'-epoxylignan (2), (8R, 8'R, 9S)-4, 4'-dihydroxy-3, 3', 9-trimethoxy-9, 9'-epoxylignan (3), (-)-pinoresinol (4), (8R, 8'R, 9'S)-4, 4'-dihydroxy-3, 3', 9'-trimethoxy-9, 9'-epoxylignan (5), (8R, 8'R, 9'R)-4, 4'-dihydroxy-3, 3', 9'-trimethoxy-9, 9'-epoxylignan (6), (9S)-9-O-methylcubebin (7), dibutylphthalate (8), piperphilippinin VI (9), balanophonin (10), and larixnaphthaone (11). Conclusion: Compounds 2-11 are isolated from the plant for the first time.
ABSTRACT
Objective To investigate the effects of dibutylphthalate (DBP) on the proliferation and apoptosis of HL-60 leukemic cells and to study its mechanism to purge leukemic cells.Methods The effects of DBP on proliferation of HL-60 leukemic cells were measured by cell culture method. The effects on apoptosis were measured by the percentage of the apoptotic cells in morphology and of the DNA fragmentation and by DNA gel electrophoresis. The intracellular free Ca~(2+) concentration ([Ca~(2+)]i) of leukemic cells were measured by Fura-2AM method. The protein expressions of c-myc and bcl-2 genes of leukemic cells were measured by immunohistochemical assay.Results DBP could suppress the proliferation of HL-60 leukemic cells in a dose-dependent and time-dependent manner and induce them to die via apoptosis.It could elicit a intracellular Ca~(2+) redistribution and a potent extracellular calcium influx. It also down-regulated the protein expressions of c-myc and bcl-2 genes of HL-60 leukemic cells.Conclusion DBP can purge (HL-60) leukemic cells in vitro by increasing [Ca~(2+)]i of cells to initiate apoptosis and down-regulating bcl-2 and c-myc proto-gene expressions to promote cell apoptosis.