Peroxiredoxin 6 Protects against Oxidative Stress and Apoptosis in a Rat Model of Lithium Chloride-Pilocarpine-Induced Epilepsy

Abstract

Background: Peroxiredoxin 6 (Prdx6) affects intracellular reactive oxygen species (ROS) and phospholipid turnover to maintain cellular homeostasis and membrane integrity. Methods: A rat model with lithium chloride-pilocarpine-induced epilepsy is employed to verify the effect and mechanism of Prdx6 on epilepsy in vivo experiments. Western blot analysis and immunofluorescence assay were used to determine the expression level of Prdx6. Furthermore, the expressions of cleaved caspase-3, Bal2 and Bax were also measured by western blot assay. The levels of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-px) were evaluated by kits. Cell apoptosis was measured through TUNEL assay. The time to onset of status epilepsy (SE), the duration of SE and the number of Racine IV or V in 28 days were recorded. Results: The results demonstrated that pilocarpine induced oxidative stress and cell apoptosis in the hippocampus of the rat epilepsy model. The expression of Prdx6 decreased with the increasing length of pilocarpine treatment in the hippocampus of rats. Prdx6 overexpression decreased spontaneous seizures in pilocarpine-treated rats. Prdx6 overexpression detained oxidative stress by reducing MDA levels and enhancing SOD, CAT and GSH-px activities in the hippocampus of rats. Furthermore, Prdx6 overexpression repressed the cell apoptosis by inhibiting the expressions of Cleaved Caspase-3 and Bax/Bcl-2 in the hippocampus of pilocarpine-treated rats. Conclusions: These findings suggest that Prdx6 can protect against oxidative stress and apoptosis in a rat model of pilocarpine-induced epilepsy, indicating that Prdx6 may be a helpful therapeutic target in treating epilepsy.