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. 2018 Jul 6;141(8):2312–2328. doi: 10.1093/brain/awy177

Figure 4.

Figure 4

GTN generates oxidative stress in trigeminal ganglion via NO and TRPA1. (A and B) Systemic (i.p.) GTN increases H2O2 levels and 4-HNE staining in trigeminal ganglion, but not in brain stem of C57BL/6 mice. (C) Two hours after GTN the increase in H2O2 in trigeminal ganglion neurons, is abolished by systemic (i.p.) cPTIO (0.6 mg/kg) and disulfiram (DSF, 100 mg/kg) (all pre-GTN) or alpha lipoic acid (αLA) or HC-030031 (HC03, both 100 mg/kg) (all post-GTN). (D) Representative images and pooled data of 4-HNE staining in trigeminal ganglion neurons, 4 h after GTN (10 mg/kg) administration in C57BL/6 mice treated systemically (i.p.) with cPTIO (0.6 mg/kg) or NAC (250 mg/kg) (all pre-GTN), or with HC03 and alpha lipoic acid (both, 100 mg/kg) (all post-GTN). (E) Systemic (i.p.) GTN (10 mg/kg) increases H2O2 levels and 4-HNE staining in trigeminal ganglion neurons from Trpa1+/+, but not Trpa1−/− mice. BL = baseline level of H2O2 or 4-HNE; Veh = the vehicle of GTN. Dash (‐) indicates combined vehicles of treatments. Error bars indicate mean ± SEM, 4–6 mice per group. *P < 0.05, **P < 0.01, ***P < 0.001; ###P < 0.001; one-way ANOVA with Bonferroni post hoc correction and Student’s t-test.