Proteome profiling of spinal cord and dorsal root ganglia in rats with trinitrobenzene sulfonic acid-induced colitis

Figure 1 The establishment of colitis in trinitrobenzene sulfonic acid rats. Representative hematoxylin and eosin microscopic photos of the colon tissue (A) revealed inflammation in the sub-mucosa layer of trinitrobenzene sulfonic acid (TNBS) rats; measurement of myeloperoxidase (MPO) activity in wet colon tissue (B, 2.61 ± 2.47 vs 0.03 ± 0.01) and tumor necrosis factor-α (TNF-α) level in colonic total protein (C, 759.80 ± 81.07 vs 174.00 ± 31.92) revealed significantly elevated MPO activity and TNF-α level in TNBS treated group in comparison with saline control group. ^aP < 0.05 vs saline group.

Figure 2 Representative examples of the silver-stained two-dimensional electrophoresis gels show expression maps of proteins in dorsal root ganglia (A) and spinal cord (B) of trinitrobenzene sulfonic acid colitis group and saline control groups. TNBS: Trinitrobenzene sulfonic acid; DRG: Dorsal root ganglia; Gstp1: Glutathione S-transferase P; Sod2: Superoxide dismutase; Ndufv2: NADH dehydrogenase (ubiquinone) flavoprotein 2; Ndufb10: NADH dehydrogenase (ubiquinone) 1 β subcomplex 10; Fh1: Fumarate hydratase; Psat1: Phosphoserine aminotransferase; Kctd12: Potassium channel tetramerisation domain containing protein 12; Vdac2: Voltage-dependent anion-selective channel protein 2; Ywhae: The 14-3-3 protein epsilon; Tst: Thiosulfate sulfurtransferase; Hspa8: Heat shock cognate 71 kDa protein.

Figure 3 Immunoblotting analyses to validate the differential expression of proteasome subunit α type-1 (A, 0. 53 ± 0.14 vs 1.81 ± 0.53) and potassium channel tetramerisation domain containing protein 12 (B, 1.21 ± 0.20 vs 0.56 ± 0.07) between trinitrobenzene sulfonic acid treated group and saline control group. The relative expression ratio standardized to β-actin. ^aP < 0.05 vs saline group. TNBS: Trinitrobenzene sulfonic acid; Psma1: Proteasome subunit α type-1; Kctd12: Potassium channel tetramerisation domain containing protein 12.

Figure 4 Schematic drawing summarizes the major findings that might associate with pathophysiological changes in rat nervous system caused by trinitrobenzene sulfonic acid-induced colitis. TNBS: Trinitrobenzene sulfonic acid; DRG: Dorsal root ganglia; Hnrnpa2b1: Heterogeneous nuclear ribonucleoproteins A2/B1; Gstp1: Glutathione S-transferase P; Prdx1: Peroxiredoxin-1; Sod2: Superoxide dismutase; Lmna: Lamin C2; Aldoa: Aldolase A; Aldoc: Aldolase C; Ckmt1: Creatine kinase, mitochondrial 1, ubiquitous; Ckm: Creatine kinase M-type; Ndufv2: NADH dehydrogenase (ubiquinone) flavoprotein 2; Ndufb10: NADH dehydrogenase (ubiquinone) 1 β subcomplex 10; Oxct1 succinyl-CoA: 3-ketoacid-coenzyme A transferase 1; Fh1: Fumarate hydratase; Mdh2: Malate dehydrogenase; Psat1: Phosphoserine aminotransferase; Cap1: Cyclase-associated protein 1; Kctd12: Potassium channel tetramerisation domain containing protein 12; Vdac2: Voltage-dependent anion-selective channel protein 2; Ywhae: The 14-3-3 protein epsilon; Tst: Thiosulfate sulfurtransferase; Stip1: Stress-induced phosphoprotein 1; Hspa8: heat shock cognate 71 kDa protein.