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A reduction in reactive oxygen species contributes to dihydromyricetin-induced apoptosis in human hepatocellular carcinoma cells.

Abstract
Reactive oxygen species (ROS) and cellular oxidant stress are considered inducers of carcinogenesis. However, the association of ROS with cancer is both complex and, at times, paradoxical. We assessed the effects of dihydromyricetin (DHM) on the induction of ROS accumulation and on the activation of the mitochondrial signaling pathway in human hepatoma HepG2 cells. The results indicated that DHM could reduce ROS accumulation in a concentration-dependent manner. Additionally, with increasing concentrations of DHM, the expression of proteins that participate in the cell apoptosis program increased in a concentration-dependent manner. Furthermore, we found that a low dose of H2O2 (10 nM) could reverse DHM-induced cell apoptosis. We observed the following critical issues: first, the cellular redox balance is vital in DHM-induced apoptosis of human hepatocellular carcinoma (HCC) cells, and second, ROS could function as a redox-active signaling messenger to determine DHM-induced cell apoptosis. In this study, we demonstrated that low levels of ROS are also critical for the function of HCC cells.
AuthorsBin Liu, Bin Lin, Xiaoyu Tan, Jian Liang, Shixing Wu, Jie Liu, Qingyu Zhang, Runzhi Zhu
JournalScientific reports (Sci Rep) Vol. 4 Pg. 7041 (Nov 13 2014) ISSN: 2045-2322 [Electronic] England
PMID25391369 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents, Phytogenic
  • Flavonols
  • Reactive Oxygen Species
  • Hydrogen Peroxide
  • dihydromyricetin
Topics
  • Antineoplastic Agents, Phytogenic (antagonists & inhibitors, pharmacology)
  • Apoptosis (drug effects)
  • Cell Line, Tumor
  • Cell Proliferation
  • Dose-Response Relationship, Drug
  • Flavonols (antagonists & inhibitors, pharmacology)
  • Hep G2 Cells
  • Humans
  • Hydrogen Peroxide (pharmacology)
  • Mitochondria (drug effects, metabolism)
  • Reactive Oxygen Species (metabolism)
  • Signal Transduction

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