Flavonoid compounds of whole plant of Crotalaria sessiliflora L / 中国药学杂志

OBJECTIVE: To investigate the flavonoid constituents of Crotalaria sessiliflora L.

Effect of monocrotaline on induction of pancreatic cancer cell BxPC-3 into polyploid giant cells / 中草药

Objective: To observe the effect of monocrotaline (MCT) extract from Crotalaria sessiliflora on inducing human pancreatic cancer cell BxPC-3 into polyploid giant cells in vitro. Methods: BxPC-3 cells (1 × 104/mL) were inoculated with MCT (0, 5, 10, and 20 μg/mL) in RPMI-1640 for 72 h, respectively, then the cell morphology was observed by Giemsa staining, and the DNA content was measured by flow cytometry; BxPC-3 cells-induced apoptosis was checked by AnnexinV-FITC/PI double staining using flowcytometry, BxPC-3 polyploid giant cell genome was checked by chromosome spreading assay, and Cyclin B1 expression also was analysed by Western blotting. Results: Giemsa staining and DNA content by flow cytometry showed that MCT induced BxPC-3 cell into polyploid giant cells in vitro. MCT treatment for 72 h appeared 4N, and 8N polyploid giant of BxPC-3 cells, induction of apoptosis, decreased the expression of cyclin B1 in a dose dependent manner. Chromosome analysis demonstrated once again that polyploid giant cell was mainly in 8N. Conclusion: Monocrotaline might exert its antitumor effect by blocking the cell cycle, inducing apoptosis, and down-regulating Cyclin B1 protein.

Study on impact of ethanol extracts from Sedum sarmentosum in inhibiting STAT-3 signaling and inducing apoptosis of human hepatocellular carcinoma cell line HepG2 / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the impact of ethanol extracts from Sedum sarmentosum (ESB) on STAT-3 signaling and its probable molecular mechanism in inducing apoptosis.</p><p><b>METHOD</b>MTT assay was used to detect the impact of ESB on HepG2 cell proliferation. FITC-Annexin V-FITC /PI double-labeling were used to investigate the impact on hepatoma carcinoma cell apoptosis. Western blot analysis was used to test the expression levels of cell apoptosis-related proteins Caspase-3, Caspase-9, PARP, P-STAT-3 (Tyr705) , STAT-3, Bcl-2, Mcl-1.</p><p><b>RESULT</b>ESB could notably inhibit proliferation of HepG2 cells, and induce HepG2 cell apoptosis, with the dose-dependent inhibitory effect. In addition, ESB could inhibit STAT-3 signaling, down-regulate Mcl-1 and Bcl-2 expressions, and induce degradation/activation of apoptosis-related proteins Caspase-3 and Caspase-9 and PARP degradation in a dose-dependent manner.</p><p><b>CONCLUSION</b>ESB inhibits HepG2 cell proliferation and induces apoptosis by inhibiting STAT-3 signaling and Mcl-1 and Bcl-2 expressions.</p>