In Vitro |
Destruxin B (1-30 μM; 48 hours) inhibits cell proliferation of H1299 cells and A549 cells, with IC50s of 4.1 μM and 4.9 μM, respectively[1]. Activation of mitochondria-dependent caspase cascade plays an important role in Destruxin B (1-30 μM; 48 hours) induced apoptotic cell death in A549 cells[1]. Destruxin B (1.25-20.00 μM; 72 hours) treatment significantly inhibits HT-29 human colorectal cancer cells viability in time- and dose-dependent manners[2]. Destruxin B (10 or 20 μM; 12 and 24 hours) treatment markedly increases levels of the proapoptotic protein PUMA and reduces levels of antiapoptotic proteins Mcl-1 of A549 cells in a concentration- and time-dependent manner [1]. Cell Proliferation Assay[1] Cell Line: H1299 cells Concentration: 1, 5, 10, 20, 30 μM Incubation Time: 48 hours Result: Inhibited H1299 cells proliferation of H1299 cells with an IC50 of 4.1 μM. Apoptosis Analysis[1] Cell Line: Lung adenocarcinoma A549 cells Concentration: 1, 5, 10, 20, 30 μM Incubation Time: 48 hours Result: Induces caspase-dependent Lung adenocarcinoma A549 cells death. Cell Viability Assay[2] Cell Line: HT-29 human colorectal cancer cells Concentration: 1.25, 2.50, 5.00, 10.00 and 20.00 μM Incubation Time: 72 hours Result: The IC50s at 24 h, 48 h and 72h were determined as 14.97, 2.00 and 0.67 μM, respectively. Western Blot Analysis[1] Cell Line: A549 cells Concentration: 10 or 20 μM Incubation Time: 12 and 24 hours Result: Regulates Mcl-1 and PUMA.
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In Vivo |
Destruxin B (DB) ( injection; 0.6-15 mg/kg/day for 6 weeks) attenuates the tumor growth in time- and dose-dependent manners[2]. Animal Model: Athymic female nude mice (BALB/cAnN.Cg-Foxn1nu/CrlNarl), approximately 4-5 weeks old on arrival[2] Dosage: Low dose (0.6 mg/kg), medium dose (3 mg/kg), high dose (15 mg/kg) Administration: Injection; daily; for 6 weeks Result: Low dose, medium dose and high dose indicated a reduction of 23.9%, 33.4% and 55.8% in mean tumor size, respectively.
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