Fig. 1

Properdin accumulates in the ischemic brain and exacerbates brain injury. a Protein expression of properdin relative to GAPDH in the ischemic hemisphere. n = 4 in sham group and 8 in the tMCAO group. ***P < 0.001 versus the sham group, one-way ANOVA with Bonferroni post hoc test. b Concentrations of properdin in the serum of tMCAO model mice. n = 5 in the sham group, 6 in the 1 d after tMCAO group, 9 in the 3 d after tMCAO group and 11 in the 7 d after tMCAO group. *P < 0.05 versus the sham group, ***P < 0.001 versus the sham group, one-way ANOVA with Bonferroni post hoc test. c The tSNE plot shows the clusters of brain cells (left, cell numbers were indicated in the parentheses) and visualizes the distribution of Cfp expression (right) after ischemic stroke. d Immunostaining for properdin and Ly6G in C57BL/6J (B6) mice 1 d after tMCAO. Scale bars: 10 µm and 50 µm. e Immunostaining for properdin, Iba-1 and TMEM119 in C57BL/6J (B6) mice 3 d after tMCAO. Yellow arrows: macrophages. Blue arrows: microglia. Scale bars: 10 µm and 50 µm. f Timeline of the experimental design. g Assessment of regional cerebral blood flow in WT and Cfp^−/− mice subjected to tMCAO. n = 5 mice per group. n.s, no significance (P > 0.05), two-way ANOVA with Sidak's multiple comparisons test. h–j Neurological deficits were evaluated by the mNSS (h), grip strength (i) and rotarod test (j) at 1 d, 3 d, and 7 d after tMCAO. n = 10 mice per group. *P < 0.05 versus the WT group, **P < 0.01 versus the WT group, two-way ANOVA with Sidak's multiple comparisons test. k The infarct area was assessed by TTC staining 1 d, 3 d, and 7 d after tMCAO. n = 8 mice per group. *P < 0.05 versus the WT group, ***P < 0.001 versus the WT group, unpaired Student’s t test. l, m Representative images and quantification of apoptotic neurons stained with TUNEL and NeuN 1 d and 3 d after tMCAO. Scale bar: 50 µm. n = 5 mice per group. *P < 0.05 versus the WT group, **P < 0.01 versus the WT group, unpaired Student’s t test