Abstract
This study investigated effects of trifluoperazine (TFP) against the cytotoxicity induced by H 2O 2 in PC12 cells and the mechanisms thereof. Different concentrations of H 2O 2 (100–500 μM) induced a significant decrease in cell viability accompanied by increased oxidative stress and cell apoptosis. Pretreatment with TFP inhibited H 2O 2-induced cell viability loss. The flow cytometric assay showed that TFP can inhibit intracellular reactive oxygen species (ROS) generation and reduce the cell apoptosis. The electrophysiological recordings indicated that when treated with H 2O 2, the calcium current was significantly increased. Pretreatment with TFP increased mitochondrial membrane potential (MMP) in cells of oxidative injury. These results suggested that TFP can reduce apoptosis by inhibiting ROS generation and preventing loss of MMP in cells. Meanwhile, the protective effect of TFP on the cell apoptosis may be related to the calcium overload. TFP may inhibit the calcium overload process to achieve the protection against apoptosis.
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