The role of endogenous reactive oxygen species in oxymatrine-induced caspase-3-dependent apoptosis in human melanoma A375 cells

Anti-cancer Drugs
Yingfan ZhangHua Jiang

Abstract

Rapid increases in incidence and mortality of human malignant melanoma are observed worldwide; thus, the development of new effective chemicals to control melanoma is urgent. In this study, the cytotoxic effect of oxymatrine, a natural quinolizidine alkaloid, against three human melanoma cell lines (A375, Sk-Mel-28, MM96L) and the underlying mechanisms were investigated. Oxymatrine killed all three human melanoma cell lines in a dose-dependent manner. The compound also dose-dependently caused apoptosis in human melanoma A375 cells. In addition, oxymatrine induced a remarkable change in mitochondrial membrane potential and triggered the release of cytochrome c from mitochondria to cytosol. Furthermore, this small compound resulted in a marked activation of capase-3, caspase-9, and poly (ADP-ribose) polymerase, while caspase-3 inhibitor Z-DEVD-FMK significantly reversed the proapoptotic effect of oxymatrine in A375 cells. Moreover, oxymatrine also dose-dependently increased the generation of reactive oxygen species in A375 cells, and N-acetylcysteine, a reactive oxygen species production inhibitor, almost completely blocked oxymatrine-induced apoptosis. In conclusion, our findings suggest that oxymatrine triggers oxidative stress...Continue Reading

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Citations

Jan 21, 2014·Acta Pharmacologica Sinica·Suo-bin Wang, Jian-ping Jia
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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis