Fig. 3

CD21 inhibited neuroinflammation and TLR4/NF-κB pathway activation in tPA-infused tMCAO mice. a–c Quantitative analysis of TNF-α, IL-1β, and IL-6 mRNA in the ipsilateral brain hemisphere, respectively. d Representative photomicrographs of GFAP-positive astrocytes and IBA-1-positive microglia/macrophages in the peri-infarct area in the ischemic brain. e-f Quantification of the fluorescence intensity (FI) of GFAP and IBA-1 in the peri-infarct area, respectively. g Representative immunoblots of TLR4/NF-κB signaling in the ipsilateral brain hemisphere. h, i Quantitative analysis of ratios of TRL4 and MyD88 to β-actin, respectively. j Quantitative analysis of the nuclear translocation ratio of NF-κB p65 to histone H3. The data are expressed as mean ± SD (n = 5/group in A-F, n = 4/group in g–j). ^#p < 0.05, ^##p < 0.01, vs. tMCAO group; *p < 0.05, **p < 0.01, vs. tPA group