Fig. 2

Injury of brain was accompanied with activation of S100B/RAGE signal and endothelial glycocalyx shedding after TBI. A Gross observation of brain tissue in TBI rats. TBI was achieved by lateral fluid percussion brain injury. B Quantification of water content of brain at different timepoints after TBI calculated with ratio of (wet weight − dry weight)/wet weight. *p < 0.05 compared with Sham group, n = 6. C Representative H&E staining images showing the histology of cortex of injured-side brain tissue at different timepoints after TBI. D Representative blots of S100B, RAGE in tissue lysates of brain peri-injury cortex at different timepoints after the onset of TBI. GADPH was used as a soluble loading control (left panel). In addition, quantification (histograms of right panels) of S100B, RAGE from representative blots shown in left panel. *p < 0.05 compared with Sham group, n = 6. E Representative blots of S100B, sRAGE in the serum of TBI rats (left panel). In addition, quantification (histograms of right panels) of S100B, sRAGE contend in serum from representative blots shown in left panel, presenting in band intensity. *p < 0.05 compared with Sham group, n = 6. F Representative confocal images showing the subcellular localization of cytocolic S100B with GFAP and the existence of membrane RAGE in GFAP⁺ cells in the cortex of injured-side brain tissue. DAPI was used as a nuclear marker. 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, n = 3