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. 2019 Jul 10;13:293. doi: 10.3389/fncel.2019.00293

FIGURE 5.

FIGURE 5

Early clenbuterol treatment promoted alternative microglia activation and suppressed neuroinflammation. (A) Clenbuterol drove microglia to an alternative activation state in sepsis mice at 24 h following CLP in the hippocampus. Representative Western blotting bands of CD68 and CD16 and CD206 and arginase1 and quantitative analysis of the relative protein levels. (C) Clenbuterol suppressed the proinflammatory response in sepsis mice at 24 h following CLP. Representative Western blots bands of CD11b and inflammatory cytokine IL-1β, TNF-α, and IL-6 and quantitative analysis of the relative protein level. (B,D) There was no significant difference in CD68, CD16, CD206, and arginase1 and IL-1β, TNF-α, IL-6 among the four groups at 16 days following CLP. Sepsis increased the expression level of CD11b at 16 days following CLP, which was reversed by early clenbuterol treatmen. N = 3 mice/group. Compared with the CLP group, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗∗p < 0.0001. All data are mean ± SEM.