Fig. 3

Activation of MCs and temporal expressions of MC-tryptase, PAR-2, p38, p-p38, and NFκB following ACA. Representative Toluidine blue staining microphotographs demonstrated that ACA promoted the activation and degranulation of brain MCs, leading to decreased number of intact, granulated MCs, less intensive staining, and the appearance of ghost cells at 24 h following the injury (a). White arrows: perivascular intact, granulated MCs. Black arrows: ghost cells. Top panel indicates the location of staining (small red box). Scale bar = 25 μm, n = 1/group. Representative western blot images (b) and quantitative analyses of endogenous MC-tryptase (c), PAR-2 (d), p38 (e), p-p38 (f), and NFκB (g) over 72 h following ACA. Significant increases in MC-tryptase, PAR-2, p38, p-p38, and NFκB, starting early after the injury and persisting until 72 h were observed in animals subjected to ACA compared to the sham group. P38 levels did not change over time. Data are expressed as mean ± SD. n = 4/group. ANOVA, Tukey. *p < 0.05 compared to sham