Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 589, Issue 1-3, Pages 27-31Publisher
ELSEVIER
DOI: 10.1016/j.ejphar.2008.04.061
Keywords
Isatin; human neuroblastoma cell; apoptosis; Bcl-2; Bax; caspase-3; vascular endothelial growth factor; mechanism
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The purpose of the study was to investigate the antitumor effects of Isatin and the related mechanism. Human neuroblastoma cells (SH-SY5Y) were exposed to Isatin at different concentrations for 48 h. Apoptotic features were demonstrated by means of nuclei staining with Hoechst 33258 and flow cytometry with Propidium Iodide (PI). Expressions of Bcl-2, Bax and Vascular endothelial growth factor (VEGF) mRNA were analyzed via RT-PCR. Expressions of Bcl-2, Bax proteins and phosphorylated extracellular signal regulated protein kinases (ERKs, p42/p44) were analyzed via Western blot. Activation of caspase-3 was assayed by flow cytometry with anti-active caspase-3-McAb-PE. VEGF protein was determined by ELISA kits. And the results showed that apoptosis of SH-SY5Y cells were induced by]satin in a close-dependent manner. Expressions of Bcl-2, VEGF mRNA and Bcl-2, VEGF proteins were clown-regulated, while expressions of Bax mRNA and Bax protein were not changed obviously. Expression of phosphorylated ERKs decreased, but the level of activated caspase-3 increased after treatment of]satin. These results suggest that Isatin promotes the apoptosis of neuroblastoma cells, therefore, it might be a potential candidate for the treatment of neuroblastoma. (C) 2008 Elsevier B.V. All rights reserved.
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