FIGURE 2.

IRI-induced local and systemic complement activation was suppressed by an individual complement gene deficiency and CRIg/FH treatment. (A–H) IRI induced extensive local complement activation in WT mice compared with Sham-operated mice, as determined by C3d (A) and MAC (E) deposition, which were remarkably suppressed by the gene deficiency of FB, C3, C4, C5, C5aR1, and C6 but not C5aR2, and CRIg/FH treatment compared with PBS control (C and G). The related quantitative results are shown in (B), (D), (F), and (H). (I–L) IRI induced extensive systemic complement activation in WT mice compared with Sham-operated mice, as determined by the serum concentrations of C3a (I) and C5a (K), which significantly declined in gene-deficient FB, C3, C4, C5, and C5aR1, but not C5aR2 or C6, mice, and CRIg/FH treatment compared with the PBS control (J and L). FB deficiency suppressed the production of C3a (I) and C5a (K) more strongly than C4 deficiency, which indicates that the alternative pathway was more relatively involved in IRI-induced complement activation than classic and MBL pathways. The related quantitative results are shown in (J) and (L). Bars represent mean ± SD (n = 5–8). ANOVA compared complement component-deficient mice, and the t test was used to compare the CRIg/FH and PBS-treated groups. *p < 0.05.