FIGURE 1.

After subarachnoid hemorrhage (SAH), blood components enter the subarachnoid space. RBC rupture hemoglobin and its metabolites, together with other damage-associated molecular patterns (DAMPs), act as inducers of the secondary inflammatory response after SAH to activate the innate immune cells (microglia and astrocytes) in central nervous system (CNS). Subsequently, immune cells such as neutrophils and macrophages in the peripheral circulation infiltrate into the injured site under the action of chemokine recruitment. These peripheral immune cells, together with innate immune cells in CNS, act as the carriers of secondary inflammation after SAH, releasing large amounts of pro-inflammatory cytokines and peroxides causing damage to neurons. Under the influence of these inflammatory products and peroxides, neurons gradually appear cell dysfunction and even apoptosis.