Fig. 4

Inhibition of S100B/RAGE signal attenuated TBI-induced up-regulation of S100B/RAGE over-expression and sRAGE secretion in astrocyte and animal models. A, B Representative blots of S100B and RAGE in injured brain, S100B and sRAGE in serum of TBI rats, or TBI plus ONO-2506 (A) or FPS-ZM-1 (B). GADPH was used as a soluble loading control (left panel). In addition, quantification (histograms of right panels) of S100B, RAGE in brain lysates and S100B, sRAGE in serum from representative blots shown in left panel. *p < 0.05 compared with Sham group, ^#p < 0.05 compared with TBI group, n = 6. C, D Representative blots of S100B and RAGE in astrocytes, S100B and sRAGE in cultured medium after stretch injury or injury plus S100B inhibitor ONO-2506 (D) or FPS-ZM-1 (E). GADPH was used as a soluble loading control (left panel). In addition, quantification (histograms of right panels) of S100B, RAGE in cell lysates and S100B, sRAGE in medium from representative blots shown in left panel. *p < 0.05 compared with Control group, ^#p < 0.05 compared with Stretch injury group, n = 3. E Representative confocal images showing the subcellular localization of S100B with GFAP and the existence of RAGE in GFAP⁺ cells in the brain tissue of rats treated with TBI, TBI plus ONO-2506 or FPS-ZM-1. Scale bar = 50 μm. The immunofluorescence intensities of S100B and RAGE in brain tissue from five fields per sample in each group were quantified and reported as relative fluorescence units (RFUs). *p < 0.05 compared with Sham group, ^#p < 0.05 compared with TBI group, n = 3