Peroxiredoxins (PRDXs) are a highly conserved family of thiol peroxidases that scavenge peroxides in cells. PRDX3 is one member of PRDXs localized in the mitochondria, and has been shown to be involved in antioxidant defense and redox signaling. In this study, we investigated the role of PRDX3 in neuronal trauma using a traumatic neuronal injury (TNI) model in primary cultured cortical neurons. We found that TNI significantly decreased the expression of PRDX3 at both mRNA and protein levels. Overexpression of PRDX3 by lentivirus (LV-PRDX3) transfection attenuated lactate dehydrogenase (LDH) release and neuronal apoptosis after TNI. The results of immunostaining showed that LV-PRDX3 transfection markedly reduced TNI-induced intracellular ROS production, protein radical formation and lipid peroxidation. In addition, overexpression of PRDX3 preserved mitochondrial membrane potential (MMP) levels and ATP generation, and inhibited mitochondrial cytochrome c release in TNI-injured neurons. The results of polymerase chain reaction (PCR) showed that PRDX3 overexpression also increased mitochondrial DNA (mtDNA) content and upregulated the expression of mitochondrial biogenesis-related factors. Taken together, our data demonstrate that PRDX3 protects against TNI insult by preserving mitochondrial function and mitochondrial biogenesis, and may have potential therapeutic value for traumatic brain injury (TBI).

过氧化物酶（PRDXs）是高度保守的硫醇过氧化物酶家族，可清除细胞中的过氧化物。PRDX3是位于线粒体中的PRDX的成员之一，并且已显示参与抗氧化防御和氧化还原信号传导。在这项研究中，我们调查了在原始培养的皮层神经元中使用创伤性神经元损伤（TNI）模型在神经元创伤中PRDX3的作用。我们发现，TNI在mRNA和蛋白质水平上均显着降低PRDX3的表达。慢病毒（LV-PRDX3）转染PRDX3的过表达减弱了TNI后的乳酸脱氢酶（LDH）释放和神经元凋亡。免疫染色的结果表明，LV-PRDX3转染显着降低了TNI诱导的细胞内ROS的产生，蛋白质自由基的形成和脂质过氧化作用。此外，c在TNI损伤的神经元中释放。聚合酶链反应（PCR）的结果表明，PRDX3的过表达还增加了线粒体DNA（mtDNA）的含量，并上调了线粒体生物发生相关因子的表达。综上所述，我们的数据表明PRDX3通过保留线粒体功能和线粒体生物发生来防止TNI侵袭，并且可能对颅脑外伤（TBI）具有潜在的治疗价值。