Figure 2.

In the earliest stage of ICH, the primary injury causes blood products (Fe2+, Hb, thrombin) to leak into the damage area to activate microglia/macrophages to express high levels of IL-6, IL-1β, TNFα, GM-CSF, INFγ, ROS, RNS, CCLs, HO-1 and MMPs. These changes extend the brain damage such as brain oedema, cell death, blood–brain barrier disruption and neurological deficits. CCLs, chemokines subfamilies; GM-CSF, granulocyte-macrophage colony stimulating factor; Hb, haemoglobin; HO-1, heme oxygenase-1; INFγ, interferon-γ; MMPs, matrix metalloproteinases; RNS, reactive nitrogen species; ROS, reactive oxygen species; TNFα, tumour necrosis factorα.