PRDX1 affects acrylamide-induced neural damage through the PTEN/AKT signaling pathway

Peroxiredoxin 1 (PRDX1) is a member of the peroxidase family of antioxidant enzymes. However, the role and mechanism of PRDX1 in acrylamide (ACR)-induced nerve damage have not been reported. We used SD rats and well-differentiated rat pheochromocytoma cells (PC-12 cells) to established in vivo and in vitro models of ACR. Immunohistochemistry, immunofluorescence and RT-qPCR experiments were used to detect the expression of PRDX1 in neurons of rat hippocampal tissue. The ultrastructural changes of neurons and PC-12 cells in rat hippocampal tissue were observed under transmission electron microscope. Western blot detected the protein expression levels of PRDX1, PTEN, AKT and p-AKT. In vivo and in vitro experimental results showed that PRDX1 showed a significant up-regulation trend after ACR exposure (p < 0.05). In vitro experiments showed that after inhibiting PRDX1 expression with PRDX1 siRNA, the survival rate of PC-12 cells significantly increased, and the damage to cell morphology and organelles was markedly improved. Western blot analysis revealed that ACR exposure can cause a significant increase in PTEN protein expression level and p-AKT/AKT protein ratio (p < 0.05). After inhibiting the expression of PRDX1, the protein expression level of PTEN and the protein ratio of p-AKT/AKT were significantly reduced, while the protein levels of SYN1 and BDNF were significantly increased (p < 0.05). This study, for the first time, demonstrates that PRDX1 affects ACR-induced neurotoxicity by regulating the PTEN/AKT signaling pathway. And, provides novel insights into the prevention and treatment of neurotoxicity in populations exposed to ACR.