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Peroxiredoxin V Protects the HT22 Cells Against NO Mediated Apoptosis
Feng Li1#, Jin Yongzhe2#, Liu Lei1, Han Bing1, Lü Chunyang1, Cui Yudong1, Sun Hunan1*
1College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing 163319, China;2School of Nursing, Yan Bian University, Yanji 133000, China
Abstract: Peroxiredoxin V (Prx V) is a thioredoxin peroxidase involved in peroxiredoxins family， which is highly expressed in neurons. Prx V is also known as reactive oxygen species (ROS) scavenger and peroxynitrite reductase， and plays a role in protecting the oxidative stress induced cell apoptosis. Excessive nitric oxide (NO) has strong neurotoxicity， could induce microglial activation and neuron cell apoptosis， which leads to neuro-degenerative diseases. It also participates in microglial activation by up-regulating the Prx V protein expression. However， the role of Prx V on NO induced hippocampal neuron cell apoptosis has yet not been clarified. In the present study， we examined the effect of sodium nitroprusside (SNP， a NO donor) on HT22 apoptosis and Prx V protein expression. We found that the SNP treatments could dose-dependently induce the HT22 cell apoptosis and selectively inhibit the Prx V protein expression， which in turn increased the cellular ROS levels， resulted in inducing the HT22 cell apoptosis. Our findings suggested the new function of Prx V on NO mediated HT22 cell apoptosis and given a hint for understanding the mechanism of NO mediated neurodegenerative diseases.
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