Subarachnoid hemorrhage (SAH) is a devastating stroke type, with high mortality and morbidity. The neuroinflammatory response evolves over time from early brain injury to delayed cerebral deterioration. Microglia, the resident immune cells of the central nervous system, respond to the acute brain injury through activation and polarization. Microglia are able to polarize along two pathways, classic M1 and alternative M2, towards tissue injury and tissue repair respectively. The modulation of microglial activation has gained appreciation as a means to prevent the detrimental effects. In this review, we describe the progression of microglial polarization after SAH and summarize the key studies on mediators of microglial activation, including M1 and M2 specific microglial markers, transcription factors and key signaling pathways. Interactions between microglia and other cells are critical in modulating microglial activation and function, which are discussed as well. The preclinical application of microglia-dependent treatments is presented, aiming for a better understanding of modulating microglial function and suggesting future investigation for therapeutic approaches.