The role of neuro-inflammatory in the pathogenesis of brain edema and hemorrhagic transformation in ischemic stroke: mechanisms and therapeutic target

Abstract

Acute cerebrovascular accident is one of the leading causes of disability and death worldwide. Given the significant increase in life expectancy of the population, stroke will remain a serious medical and social problem in the next few decades. Among the various causes of stroke, ischemic brain damage predominates. Ischemic stroke is based on a decrease in the intensity of blood supply to the brain tissues, as a result of which there is a decrease in the delivery to neurons of the required amount of glucose and oxygen, which are required to ensure the normal function of this organ. At the same time, in many cases, spontaneous or medical restoration of blood flow after a period of ischemia is accompanied by a paradoxical increase in damage, and therefore it is advisable to consider the process of damage to brain tissue during circulatory disorders in the context of ischemic-reperfusion injury (IRI). One of the key mechanisms of brain IRP is the inflammatory response. In the process of secondary immune damage to the brain, both mechanisms of innate immunity, manifested by leukocyte infiltration of the damaged brain area, and antigen-dependent reactions of adaptive immunity are involved. One of the most important manifestations of neuroinflammation in cerebral IRI is an increase in transand paracellular permeability of the blood-brain barrier, which underlies the development of vasogenic cerebral edema and hemorrhagic transformation of the focus. This review considers current ideas about the molecular mechanisms that link aseptic inflammation, edema, and hemorrhagic transformation.