Oxidative stress plays a role in many neurological diseases. Hypoxic preconditioning (HPC) has been proposed as an intervention that protects neurons from damage by altering their response to oxidative stress. The aim of this study was to investigate the mechanisms by which HPC results in neuroprotection in cultured SH-SY5Y cells subjected to oxidative stress to provide a guide for future investigation and targeted interventions. SH-SY5Y cells were subjected to HPC protocols or control conditions. Oxidative stress was induced by HO. Cell viability was determined via adenosine triphosphate assay. Rapamycin and 3-methyxanthine (3-MA) were used to induce and inhibit autophagy, respectively. Monodansylcadaverine staining was used to observe the formation of autophagosomes. Levels of Microtubule-associated protein light chain 3 B (LC3B), Beclin 1, and p53 were measured by Western blot. Reactive oxygen species (ROS) were also determined. Cell viability in the HPC group following 24-h exposure to 600 μM HO was 65.04 ± 12.91% versus 33.14 ± 5.55% in the control group. LC3B, Beclin 1, and autophagosomes were increased in the HPC group compared with controls. Rapamycin mimicked the protection and 3-MA decreased the protection. There was a moderate increase in ROS after HPC, but rapamycin can abolish the increase and 3-MA can enhance the increase. p53 accumulated in a manner consistent with cell death, and HPC-treated cells showed reduced accumulation of p53 as compared with controls. Treatment with rapamycin decreased p53 accumulation, and 3-MA inhibited the decrease in p53 induced by HPC. HPC protects against oxidative stress in SH-SY5Y cells. Mechanisms of protection may involve the activation of autophagy induced by ROS generated from HPC and the following decline in p53 level caused by activated autophagy in oxidative stress state. This is in line with recent findings in nonneuronal cell populations and may represent an important advance in understanding how HPC protects neurons from oxidative stress.
Objective To compare changes in foraminal motion at two time points post-surgery between artificial disc replacement (ADR) and anterior cervical discectomy and fusion (ACDF). Methods Eight ACDF and 6 ADR patients (all single-level C5-6) were tested at 2 years (T1) and 6.5 years (T2) post-surgery. The minimum foraminal height (FH.Min) and width (FW.Min) achieved during neck axial rotation and extension, and the range of these dimensions during motion (FH.Rn and FW.Rn, respectively) were measured using a biplane dynamic x-ray system, CT imaging and model-based tracking while patients performed neck axial rotation and extension tasks. Two-way mixed ANOVA was employed for analysis. Results In neck extension, significant interactions were found between year post-surgery and type of surgery for FW.Rn at C5-6 (p<0.006) and C6-7 (p<0.005), and for FH.Rn at C6-7 (p<0.01). Post-hoc analysis indicated decreases over time in FW.Rn for ACDF (p<0.01) and increases in FH.Rn for ADR (p<0.03) at the C6-7 adjacent level. At index level, FW.Rn was comparable between ACDF and ADR at T1, but was smaller for ACDF than for ADR at T2 (p<0.002). In axial rotation, differences were found between T1 and T2 but did not depend on type of surgery (p>0.7). Conclusions Changes were observed in the range of foraminal geometry at adjacent levels from 2 years to 6.5 years post-surgery that were different between ACDF and ADR for neck extension.
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