The major findings of this study are as follows (Figure 10): (1) C1q/C3-CR3 signaling was active with time after ICH; (2) activation of CR3 exacerbated ICH-induced brain injury; (3) CR3 activation upregulated CD163/HO-1 expression and promoted hematoma resolution after ICH; (4) oral minocycline treatment had neuroprotective effects on brain injury after ICH partly by downregulating C1q and CR3; and (5) the effect of oral minocycline on post-ICH brain injury can be reversed by potentiating CR3. Here, C3 is linked to hematoma.