P53-Induced ROS-Accumulation Induces Programmed Cell Death by Nano-Liposome of Quercetin in C6 Glioma Cells

Purpose: As one of the major types of programmed cell death (PCD), necrosis has been demonstrated to be responsible for cell death and the mechanisms responsible for necrosis are still not very clear. This study investigates nano-liposome of quercetin induced programmed cell death (PCD), including apoptosis and necrosis for C6 glioma cells by regulating p53-induced accumulation of reactive oxygen species (ROS) and mitochondrial membrane potential(MMP). Methods: The C6 glioma cells were treatment with nano-liposome of quercetin (QUE-NL) and assayed for cell survival, cellular ROS and MMP levels by flow cytometry assays, and western blot assay P53, cytochrome C release and caspase activations expression. The C6 glioma cells pretreated with p-53 inhibitor-alpha(PFT-alpha) and N-acetylcysteine (NAC) to measure ROS level and p53 expression respectivly. Results: C6 glioma cells showed a significant decrease in DHE-fluorescence beginning at 24h treatment, Which treated nano-liposome of quercetin. Interestingly, the accumulation of ROS was elevated With P53 expressing in C6 glioma cells. The increase in ROS levels was followed by a decrease in cell growth and viability, MMP was decline and increase in the percentage of cells with necrosis. Conclusions: p53 overexpression enhanced p53-induced ROS-accumulation within 24h treatment, which was accompanied with a decrease in cytochrome c and caspase-3,9 protein levels. These results support the hypothesis that after the nano-liposome of quercetin regulates p53-induced ROS -accumulation apoptosis and necrosis of C6 glioma cells.