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. 2019 Nov 15;13:1223. doi: 10.3389/fnins.2019.01223

FIGURE 8.

FIGURE 8

TLR4 deficiency enhanced the effects of curcumin on microglia phenotype switch into M2 at 24 h after SAH. (A) Western blotting showed that TLR4 deficiency reduced the protein levels of TLR4 (B) and CD86 (C) post SAH as compared with the wild type (WT) SAH group, and increased the expression of CD206 (D). Curcumin treatment in tlr4–/– group further elevated the level of CD206 as relative to the tlr4–/– SAH group and had no statistic difference on TLR4 and CD86. (E–H) ELISA showed that the contents of IL-1β (E), IL-6 (F), TNF-α (G), and IL-10 (H) significantly changed in tlr4–/– SAH group compared with the WT SAH group, and curcumin treatment in tlr4–/– mice further suppressed the release of pro-inflammation cytokines (IL-1β and TNF-α) and increased the level of IL-10 as relative to the tlr4–/– SAH group. (I,J) Curcumin treatment in tlr4–/– mice had no significant difference on brain water content and neurological score as relative to the tlr4–/– SAH group and WT SAH + Cur group. The quantitative data are the mean ± SD (n = 9, each; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 vs. WT SAH group; #p < 0.05, ##p < 0.01 vs. WT SAH + Cur group; @p < 0.05 vs. tlr4–/– SAH group; nsp > 0.05).