Research progress of endogenous hematoma absorption after intracerebral hemorrhage

Abstract

Non-traumatic intraparenchymal brain hemorrhage is referred to as intracerebral hemorrhage (ICH). Although ICH is associated with a high rate of disability and case fatality, active intervention can significantly lower the rate of severe disability. Studies have shown that the speed of hematoma clearance after ICH determines the patient's prognosis. Following ICH, depending on the hematoma volume and mass effect, either surgical- or medication-only conservative treatment is chosen. The goal of promoting endogenous hematoma absorption is more relevant because surgery is only appropriate for a small percentage of patients, and open surgery can cause additional trauma to patients. The primary method of removing hematoma after ICH in the future will involve understanding how to produce and manage macrophage/microglial endogenous phagocytic hematomas. Therefore, it is necessary to elucidate the regulatory mechanisms and key targets for clinical purposes.

Keywords: haematoma absorption; intracerebral hemorrhage; microglia; phagocytosis; scavenger receptor.

Figure 1

The blood chemical components of coagulation following intracerebral hemorrhage mainly include red blood cells, hemoglobin, and heme, which are mediated by CD36, CD163, and CD91 expressed on phagocytes, respectively.

Figure 2

Microglia surrounding hematomas after intracerebral hemorrhage are polarized to an M1 or M2 phenotype. M1 phenotype promotes inflammation. M2 inhibits inflammation and promotes phagocytosis. The hematoma component is engulfed by M2 microglia, which mainly increases the expression of proteins related to phagocytosis under the action of PPAR-γ and Nrf2 signaling pathways and relieves the cytotoxicity of metabolites after phagocytosis of hematoma components. Simultaneously, M1 is inhibited by some other drugs to promote the polarization of M2 microglia.