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. 2009 Dec 30;133(1):126–138. doi: 10.1093/brain/awp304

Figure 6.

Figure 6

Altered SLPI, Iκ-Bα, and cytokine levels in the spinal cord of recombinant mouse SLPI-treated mice after spinal cord injury. (A) Western blots for SLPI and Iκ-Bα show increased levels of both proteins in the spinal cord of mice 12 and 24 h, respectively, after spinal cord injury in mice injected with recombinant mouse SLPI, as compared to vehicle-treated controls. β-actin is used as a loading control (n = 3 per group). (B) Micrographs of small rounded SLPI+ cells ∼10–12 μm in diameter (arrows in panels i–iii) that appear to be leukocytes located in the dorsal injured part of the spinal cord from mice 12 h after recombinant mouse SLPI injection and spinal cord injury. In panel (iv) SLPI+ cells (arrows) are seen on the outer side of blood vessels that may be cells that have migrated out of the circulation. Scale bar = 15 µm. (C) Quantitative real-time PCR analysis of mRNA expression of pro-inflammatory chemokine and cytokine expression 12 h after spinal cord injury shows a significant reduction in TNF-α mRNA levels (*P < 0.05; n = 3 per group) in mice treated with recombinant mouse SLPI. No changes are seen in monocyte chemotactic protein-1, IL-6 and IL-1β mRNA levels (n = 3 per group). Data represent fold increase over vehicle-treated controls (horizontal line) also taken 12 h after spinal cord injury.