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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Anti-inflammatory and immunomodulatory mechanisms of atorvastatin in a murine model of traumatic brain injury

Fig. 2

Effect of atorvastatin treatment on brain immune cell subsets after TBI. a Representative gating strategy of isolating microglia (CD11b+CD45low), macrophages (CD11b+CD45highLy6G), neutrophils (CD11b+CD45highLy6G+), total T cells (CD45+CD3+), B cells (CD45+B220+), and NK cells (CD45+NK1.1+) infiltrating the brain. bg Quantitative analysis of the invading cellular components in the different groups. Flow cytometric analysis showed a significant decline in microglia (b), macrophages (c), and T cells (b) in the atorvastatin group compared with the saline group at 72 h post-TBI. Atorvastatin administration had no effect on B cells (f) at 24 and 72 h following TBI. At 24 and 72 h post-TBI, atorvastatin treatment led to a significant reduction in the recruitment of neutrophils (d) and NK cells (g) to the injured brain when compared to the saline group. Data are presented as the mean ± SD. **p < 0.01 and ***p < 0.001 versus sham group, # p < 0.05, ## p < 0.01, and ### p < 0.001 versus TBI + saline group. n = 6/group. FSC-A = forward scatter channel area, SSC-A = side scatter channel area, FITC = fluorescein isothiocyanate, PE = phycoerythrin, and APC = allophycocyanin

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