Abstract
Chinese herb Radix sophorae is widely applied as an anticarcinogenic/antimetastatic agent against liver cancers. In the current study, Sophoraflavone J, a flavonoid constituent enriched in the root of Radix sophorae, induced apoptosis in human hepatoma HepG2 cells via the intrinsic mitochondrial death pathway. The molecular mechanism of the cytotoxic effect was further investigated by a comparative proteomic approach. Differentially expressed proteins identified included membrane proteins/antigens, structural proteins, transcriptional factors, glycolytic enzymes, heat-shock chaperon proteins, ROS-related proteins and proteosomes, etc. These findings were further validated by Western blot analysis and real-time PCR. Preliminary experiments to characterize the roles of these proteins were conducted. Our data suggested that Sophoraflavone J treatment triggered nutrient depletion and generation of ROS in cells, which subsequently led to mitochondrial dysfunction and apoptosis.
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