Saturday, January 14, 2012
Cancer and betulinic acid article, please explain this article?
Studies have shown that betulinic acid can induce apoptosis in neuroectodermal tumors, and this betulinic acid-induced apoptosis was independent of CD95-ligand/receptor interaction and aculation of wild-type p53 protein, but dependent on activation of caspases (interleukin 1ß-converting enzyme/Ced-3-like proteases). The broad-spectrum peptide inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluorometh… which blocked of FLICE and PARP, also completely abrogated BA-triggered apoptosis. Overexpression of Bcl-2 and Bcl-xl conferred resistance to BA at the level of mitochondrial dysfunction, protease activation, and nuclear fragmentation. This suggested that mitochondrial alterations were involved in BA-induced activation of caspases. Furthermore, Bax and Bcl-xs, two death-promoting proteins of the Bcl-2 family, were up-regulated following BA treatment. Most importantly,neuroblastoma cells resistant to CD95- and doxorubicin-mediated apoptosis were sensitive to treatment with BA
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