Sulfiredoxin-1 protects spinal cord neurons against oxidative stress in the oxygen-glucose deprivation/reoxygenation model through the bax/cytochrome c/caspase 3 apoptosis pathway

Abstract

BackgroundSpinal cord ischemia/reperfusion injury is a common clinical, pathophysiological phenomenon with complex molecular mechanisms. Currently, there are no therapeutics available to alleviate the same. This study investigates the protective effects of sulfiredoxin-1 (Srxn 1) on spinal cord neurons following exposure to oxygen-glucose deprivation/reoxygenation (OGD/R) treatment. Materials and methodsPrimary spinal cord neurons were cultured, detected by anti-tubulin βⅢ, and transfected with adeno-associated virus (AAV)-Srxn 1 to overexpress Srxn 1. They were identified by their morphology and CCK-8 assay. The superoxide dismutase level was measured by superoxide dismutase assay. Malondialdehyde level was measured by malondialdehyde assay. The apoptosis ratio was calculated by Hoechst 33342 and Annexin V-PE/7-AAD staining. Mitochondrial transmembrane potential (Δψm) was detected by tetramethylrhodamine-methyl ester-perchlorate (TMRM) staining. The mRNA expression levels of Srxn 1 and caspase 3 were detected by quantitative reverse transcription-polymerase chain reaction, and the protein expression levels of Srxn 1, bax, bcl-2, cytosolic cytochrome c, and caspase 3 were detected by western blotting. ResultsAAV-Srxn 1 up-regulated mRNA and protein levels of Srxn 1 in spinal cord neurons. Following exposure to OGD/R, overexpression of Srxn 1 improved the neuronal viability, alleviated the neuron apoptosis, enhanced the mitochondrial transmembrane potential, increased the SOD level, decreased the MDA level, inhibited the expression of cytosolic cytochrome c, bax, and caspase 3, and promoted the expression of bcl-2. ConclusionSrxn 1 plays a significant role in anti-apoptosis of spinal cord neurons, and Srxn 1 may be a potential therapeutic target for spinal cord I/R injury.