Abstract
1. Accumulated clinical evidence suggests that selective oestrogen receptor modulators (SERM), such as raloxifene, may be neuroprotective. Oxidative stress is a likely molecular mechanism in the neurotoxicity of kainic acid (KA), an excitotoxic substance. The expression levels of the apurinic/apyrimidinic endonuclease/redox factor-1 (APE/Ref-1) gene seem to correlate with cellular sensitivity to reactive oxygen species (ROS) and a reduction in the expression of APE/Ref-1 may cause oxidative DNA damage. 2. The aim of the present study was to assess the effects of KA and raloxifene on the level of APE/Ref-1 mRNA in the hippocampus of ovariectomized rats. The expression of the APE/Ref-1 gene was quantified using reverse transcription followed by real-time polymerase chain reaction. 3. The results show that the level of APE/Ref-1 mRNA increased significantly in raloxifene-treated rats. However, raloxifene treatment did not affect the seizure severity induced by KA. We also observed that raloxifene treatment against simultaneous KA injection maintained the increased level of APE/Ref-1 mRNA in the hippocampus. 4. Therefore, the results of the present study seem to support previous data suggesting the potential significance of raloxifene in neuroprotection.
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