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. 2020 May 11;17:154. doi: 10.1186/s12974-020-1731-x

Fig. 10.

Fig. 10

Exogenous TSG-6 inhibited the expression of pro-inflammatory cytokines and suppressed the TLR2/MyD88/NF-κB signaling pathway in Pam3CSK4-treated primary microglia. ac Recombinant TSG-6 inhibited the increased mRNA levels of IL-1β, IL-6, and TNF-α in Pam3CSK4-treated primary microglia in a concentration-dependent manner. df Recombinant TSG-6 inhibited the release of IL-1β, IL-6, and TNF-α in Pam3CSK4-treated primary microglia in a concentration-dependent manner. g Representative image of protein levels of TLR2, MyD88, p-p65, p65 in primary microglia. hk Quantitative analysis of the Western blot result showed that recombinant TSG-6 inhibited the Pam3CSK4-induced up-regulation of TLR2, MyD88, p-p65 protein expression in primary microglia in a concentration-dependent manner. l Typical micrographs of immunocytochemical staining are shown for the cytoplasmic and nuclear distribution of NF-κB p65. Scale bar: 30 μm; 10 μm (magnified graphs). The data are expressed as the means ± SD (n = 8 in each group). **P < 0.01 versus the control group. #P < 0.05, ##P < 0.01 versus the Pam3CSK4 group. Statistical significance was determined by one-way analysis of variance (ANOVA) with post hoc Tukey test