Résumé
Intracerebral hemorrhage is the bleeding caused by spontaneous non-traumatic rupture of blood vessels in brain parenchyma. It has high disability rate and mortality. A series of injuries after intracerebral hemorrhage will lead to neuronal apoptosis. If apoptotic neurons are not cleared in time, intracellular toxic substances will be released, thereby further aggravating the inflammatory reaction. Therefore, the timely clearance of apoptotic cells is of great significance to the brain homeostasis after intracerebral hemorrhage. At the same time, a large number of phagocytic "eat me" signal phosphatidylserine (PS) will appear on the surface of apoptotic neurons. Microglia, as resident macrophages in the brain, have a variety of PS receptors on their surface, which promote the phagocytosis of apoptotic neurons by microglia and reduce the occurrence of local inflammatory responses.
Résumé
The disability and mortality rate of patients with intracerebral hemorrhage are very high. At present, there is no effective treatment to improve the outcome of patients with intracerebral hemorrhage. Mechanical compression of hematoma and release of toxic products are the main causes of primary and secondary brain injury in patients with intracerebral hemorrhage, while safe and effective acceleration of hematoma regression is the key strategy to improve the neurological deficit in patients with intracerebral hemorrhage. Microglia/macrophages are the main phagocytic system that mediates hematoma clearance and are mainly polarized into M1 and M2 phenotypes. Cell surface receptors and possible signal transduction pathways play an important role in regulating the endogenous hematoma regression mediated by microglia/macrophages, and may become a new target for clinical treatment of intracerebral hemorrhage and improvement of the outcomes of patients in the future.