Spontaneous intracerebral hemorrhage (ICH) accounts for approximately 10–15% of all strokes with high rates of mortality and residual disability. Multiple studies have demonstrated that microglia-mediated neuroinflammation exerts a significant function on the secondary injury of ICH, which may cause severe brain damage or potential neurorestoration in different conditions. Microglia are the major phagocytes in central nervous system. In different time courses after ICH, microglia can be activated and polarized into two different states: classic M1-like phenotypes in the early stage and alternative M2-like phenotypes in long-term recovery. The mechanism of this phenotypic change is very complicated, including the influence of inflammatory mediators and microglia-astrocyte crosstalk. In this work, we encapsulate the M1-to-M2 microglial phenotype transition as well as its effects on post-ICH neuroinflammation, and describe potential therapeutic targets based on this feature.