Fig. 4

Neuroinflammation in spinal cord tissue rostral to the epicenter. A Immunoreactivity level (IRL) of GFAP (reactive astrogliosis), Iba-1/(microglia/macrophage activation), TNF-α (proinflammatory cytokine), and/or iNOS (marker of proinflammatory microglia/macrophage; inflammation mediator) expressions were evaluated in coronal sections sampled from T8 spinal cord (SCI group) or T10 level (control group). B Specific areas in each section that were examined by IHC assay (for specific data point, please see individual images accordingly labeled in C–Q). In the dorsal horn (DH; C–F₁) and dorsal column (DC; G–J₁), there were significantly increased expressions of GFAP (DH: C, D; DC: G, H) and iNOS (DH: C, D₁; DC: G, H₁) in injured spinal cords, compared to the control tissue (DH: C₁; DC: G₁). Also significantly heightened in the dorsal spinal cord were expressions of TNFα (DH: E, F; DC: I, J) and Iba-1 (DH: E, F₁; DC: I, J₁; controls: E₁/DH and I₁/DC; n = 4/group; p < 0.01; Student’s t test). In addition, compared to control sections, the lateral column (LC) and ventral funiculi (VF) of SCI tissues showed significant IRL augmentations of GFAP (LC: K, L; VF: O, P), iNOS (LC: K, L₁; VF: O, P₁), TNFα (LC: M, N; VF: Q, R), and Iba-1 (LC: M, N₁; VF: Q, R₁; controls: K₁, M₁ for LC and O₁, Q₁ for VF; n = 4/group; p < 0.01; Student’s t test; scale bars: 40 µm/C, G; 60 µm/K, O)