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The role of reactive oxygen species in epigallocatechin-3-gallate-induced apoptosis of human gastric cancer MGC803 cells / 中国癌症杂志
China Oncology ; (12)2001.
Article in Zh | WPRIM | ID: wpr-548684
Responsible library: WPRO
ABSTRACT
Background and purpose:Anticancer mechanism of epigallocatechin-3-gallate(EGCG)remains unclear.This study investigated the role of reactive oxygen species(ROS)in epigallocatechin-3-gallate(EGCG)-induced apoptosis in human gastric cancer MGC803 cells.Methods:The inhibition of MGC803 cells growth was measured by MTT assay.Apoptosis of MGC803 cells was studied by using the AO/EB fluorescence stain.Flow cytometry was used to detect the intracellular ROS level and the rate of apoptosis.Results:EGCG could induce apoptosis of MGC803 cells and increased in the intracellular ROS level.However,after treatment with N-acetyl-L-cystein and an athiol-containing antioxidant,the inhibitory effect of EGCG on MGC803 cells was significantly weakened.The apoptotic rate of the cells and the activity of the intracellular ROS level also decreased dramatically.Conclusion:EGCG can induce apoptosis of MGC803 cells.In turn,the ROS inhibitor can significantly inhibit the apoptosis induced by EGCG in MGC803 cells.These results suggest that the cellular generation of ROS plays a role in initiating EGCG-mediated apoptosis of MGC803 cells.
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Full text: 1 Index: WPRIM Language: Zh Journal: China Oncology Year: 2001 Type: Article
Full text: 1 Index: WPRIM Language: Zh Journal: China Oncology Year: 2001 Type: Article