FIG. 7.

Valproic acid (VPA) inhibits endoplasmic reticulum (ER) stress-associated caspase-12 activation after spinal cord injury. Spinal tissues and protein extracts given with and without VPA were prepared at the indicated time points (4 h, 8 h, 1 day, and 3 days after injury) as described in the Methods section (n=3/group). Total protein (50 μg) was analyzed by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis (PAGE) and subjected to Western blot with anti-cleaved caspase-12 antibody (A). Spinal tissues 1 mm rostral from lesion site prepared at 4 h after injury were processed for double immunofluorescence staining with anti-caspase-12 and anti-NeuN antibodies (B). Note that cleaved caspase-12 was co-localized with neurons, especially ventral motor neurons (VMN) after SCI. Scale bar, 30 μm. (C) Western blot (upper) and quantitative analysis (bottom) of cleaved caspase-12 with total protein prepared at 4 h after injury. Note that VPA significantly inhibited the level of cleaved caspase-12 as compared with vehicle control. Data are presented as means±SD. *p<0.05. Color image is available online at www.liebertpub.com/neu