Figure 4.

BAY protects the neurovascular unit in the mouse controlled cortical impact-indued TBI model. (A) TBI mice were administrated with BAY (3 mg/kg) for 7 days before the density of neuronal cells and oligodendrocytes in the surrounding lesion area were assessed by IF staining. Scale bar, 50 µm (MBP, green; NeuN, red; DAPI, blue). (B) Quantification of NeuN and MBP expression. (C) Cerebrovascular damage in the surrounding lesions in mice after TBI induction was assessed by IF staining. Scale bar, 50 µm (CD31, red; DAPI, blue). (D) Changes in astrocytes in the surrounding lesions in TBI mice were tested using IF. Scale bar, 50 µm (GFAP, green; DAPI, blue). (E) Expression of the tight junction marker protein Claudin-5 in mouse brain tissues was detected via western blotting. (F) Viability of PC12 cells co-cultured with MG treated with CCE was determined using Cell Counting Kit-8. (G) mRNA expression levels of apoptosis markers Bax and Bim were detected via reverse transcription-quantitative PCR. (H) Bax protein expression was detected via western blotting. ^*P<0.05, ^**P<0.01, ^***P<0.001, ^****P<0.0001. BAY, BAY61-3606; TBI, traumatic brain injury; IF, immunofluorescence; NeuN, neuronal nuclear protein; GFAP, glial fibrillary acidic protein; MBP: myelin basic protein; MG, microglia; CCE, cerebral cortex extract.