Figure 8

Effect of PPAR-α on the anti-inflammatory property of simvastatin on NF-κB activation after SCI. Citoplasmatic IκB-α and nuclear p65 NF-κB levels were detected in the spinal cord from sham and injured-PPAR-αKO mice and PPAR-αWT mice treated or not with simvastatin. A basal level of IκB-α was detected in the spinal cord tissues from sham WT mice (a) and from sham PPAR-α KO mice (a), whereas IκB-α levels were substantially reduced after SCI and significantly in PPAR-αKO mice (a). Simvastatin treatment, instead, increased IκB-α levels in both mice group but significantly more in WT treated mice (a). In addition, SCI caused a significant increase in nuclear NF-κB p65 compared to the sham-operated mice (b) and these increase was higher in SCI PPAR-αKO mice (b) than sham PPAR-αWT mice (b). Simvastatin treatment (10 mg/kg at 1 and 6 h after SCI induction) significantly reduced NF-κB p65 levels much more in WT treated mice (b) than PPAR-αKO mice (b). Polyclonal actin and lamin were used as internal control. The bars of each western blot are represented a densitometry analysis expressed as mean ± S.E.M. of three different experiments. *P < 0.01 vs. sham; °P < 0.01 vs. SCI-WT group; #P < 0.01 vs. simvastatin-treated group.