ABSTRACT
OBJECTIVE: The role of antioxidant in cancer cell proliferation is still controversial. This study aimed to explore the effects of antioxidant vitamin E on the proliferation of breast cancer cells and the possible underlying mechanisms. MATERIALS AND METHODS: Orthotopic breast cancer model was established by inoculating MCF7 cells in mice and in vitro MCF7 culture system. CM-H2DCFDA fluorescence probe and Western blot analysis were used to detect ROS changes and p53 expression. p53 knockdown in MCF7 cells by siRNA transfection was also used to determine the combination effect of vitamin E and p53 on MCF7 cell proliferation. RESULTS: Vitamin E supplement in the chow significantly accelerated breast cancer cell growth in vivo. ROS level and p53 expression were decreased in tumor tissues. Water-solvable vitamin E Trolox significantly promoted MCF7 cell proliferation in vitro, while reducing intracellular ROS level and p53 expression. p53 knowdown by p53-siRNA transfection inMCF7 cells significantly reduced p53 expression and increased MCF7 cell proliferation. CONCLUSIONS: Vitamin E accelerated breast cancer growth by reducing ROS production and p53 expression.
Subject(s)
Antioxidants/pharmacology , Breast Neoplasms , Reactive Oxygen Species/metabolism , Tumor Suppressor Protein p53/metabolism , Vitamin E/pharmacology , Animals , Breast Neoplasms/metabolism , Breast Neoplasms/pathology , Cell Proliferation/drug effects , Humans , MCF-7 Cells , MiceABSTRACT
OBJECTIVE: We used a rabbit model of hepatic ischemia reperfusion in situ to observe the change of portal venous endotoxin level before reperfusion, and the effect of portal blood stasis removal on intestinal endotoxemia and hepatic ischemia reperfusion injury. The purpose was to find an ideal method for portal blood stasis removal and provide the experimental proof for clinical application of hepatectomy. METHODS AND MATERIALS: To investigate the effect of portal blood stasis removal on intestinal endotoxemia and hepatic ischemia reperfusion injury, a rabbit hepatic ischemia reperfusion injury model was established and treated with removal of portal blood stasis before the portal blood circulation was resumed. Serum endotoxin content, alanine aminotransferase (ALT), hyaluronic acid (HA), and content of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD) and activation of nuclear factor-κB (NF-κB) in liver tissue were examined respectively. RESULTS: In portal blood stasis the level of serum endotoxin significantly decreased with each 2.5 mL blood removal (P < .01), subsequently reaching a minima at the 7.5 mL blood removal (P > .05). Removing portal blood stasis ameliorated endotoxemia and hepatic ischemia reperfusion injury as shown by ALT, HA, MDA, SOD, TNF-α, IL-6, and activation of NF-κB compared to no removal. The first 5 mL portal blood stasis contains high volume of endotoxin which may be responsible for hepatic reperfusion injury. CONCLUSION: Removal of portal blood stasis before the resume of splanchnic circulation may ameliorate intestinal endotoxemia and hepatic ischemia reperfusion injury.
