Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

Figure 4

Oxidative stress induces neuronal autophagic cell death in SCIR injury. (a) Immunofluorescence analysis of ROS in the spinal cord after SCIR treated with or without NAC. (b) MDA concentration and (c) SOD activity in the spinal cord after I/R treated with or without NAC. (d) Immunofluorescence analysis of TUNEL and LC3 in the spinal cord after I/R treated with or without NAC. (e) Immunofluorescence analysis of caspase-3 in the spinal cord after I/R treated with or without NAC. (f) Western blot analysis of p62, Atg12-5, LC3-II, and cleaved caspase-3 after I/R injury treated with or without NAC. (g) Densitometric analysis of the immunoblot reported in Figure 4(f). (h) BBB scores of animals after SCIR treated with or without NAC. Images represent six rats with I/R treated with or without NAC. Scale bars represent 10 μm. . Data were analyzed using one-way ANOVA in (b), (c), and (g) and two-way ANOVA in (h). Data represent three independent experiments. SCIR: spinal cord ischemia reperfusion; ROS: reactive oxygen species; NAC: N-acetyl-L-cysteine; MDA: malondialdehyde; SOD: superoxide dismutase; I/R: ischemia reperfusion; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling; BBB: Basso, Beattie, and Bresnahan; ANOVA: analysis of variance.

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