FIG. 3.

Inhibition of astrocyte activation by edaravone. (A) Representative immunohistochemistry staining of microtubule proteins expressed following astrocyte activation, GFAP (a–c), vimentin (d–f), and S-100 (g–i), in brain tissue surrounding the contusion site are upregulated following TBI in vehicle-treated rats (b, e, and h) compared to sham-operated (a, d, g). and edaravone-treated (c, f, i) rats. (B–D) Quantification of cells positive for GFAP-, vimentin-, and S-100, respectively. (E–G) Representative Western blots of GFAP, vimentin, and S-100, respectively with semi-quantification data for each protein relative to β-actin directly underneath the representative blot. Bars represent mean±standard deviation. n=4 rats/group for all experiments. *p<0.05, **p<0.01, vs. sham group; ^##p<0.01, vs. vehicle group. Edv, edaravone-treated group; GFAP, glial fibrillary acidic protein; Veh, Vehicle-treated group; Vim, vimentin. Scale bar=50 μm. Color image is available online at www.liebertonline.com/neu