Intracerebral haemorrhage: from clinical settings to animal models

Abstract

Spontaneous intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity and for which no effective treatments are available to date. Much experimental and clinical research have been performed to explore its mechanisms regard the subsequent inflammatory cascade and to seek the potential therapeutic strategies. The aim of this review is to discuss insights from clinical settings that have led to the development of numerous animal models of ICH. Some of the current and future challenges for clinicians to understand ICH are also surveyed.

Keywords: inflammatory response; stroke.

Figure 1

Risk factors of ICH. (A) Risk factors of ICH. (B) Some clinical diseases that can cause ICH. ICH, intracerebral haemorrhage.

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.