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

Figure 5

H₂S inhibits neuronal autophagic cell death after SCIR injury. (a) Immunofluorescence analysis of ROS in the spinal cord after I/R treated with or without H₂S. (b) MDA concentration and (c) SOD activity in the spinal cord after I/R treated with or without H₂S. (d) Immunofluorescence analysis of TUNEL and LC3 in the spinal cord after I/R treated with or without H₂S. (e) Immunofluorescence analysis of caspase-3 in the spinal cord after I/R treated with or without H₂S. (f) Western blot analysis of cleaved caspase-3, Bax, BLC2, LC3, Atg12-Atg5, p62, p-AKT, and p-mTOR in the spinal cord extracts from normal and I/R rats treated with or without H₂S. (g) Densitometric analysis of the immunoblot reported in (f). (h) BBB scores of animals after SCIR treated with or without H₂S. Images represent six rats with I/R treated with or without H₂S. Scale bars represent 10 μm. . Data were analyzed using one-way ANOVA in (b), (c), and (g) and two-way ANOVA in (h) and represent three independent experiments. H₂S: hydrogen sulfide; SCIR: spinal cord ischemia reperfusion; ROS: reactive oxygen species; I/R: ischemia reperfusion; MDA: malondialdehyde; SOD: superoxide dismutase; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling; LC3: microtubule-associated protein 1 light chain 3; BBB: Basso, Beattie, and Bresnahan; ANOVA: analysis of variance.

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