PHAGOCYTOSIS ACTIVATION IN THE RAT BRAIN IN THE CONDITIONS OF ACUTE SOMATOGENIC TOXIC ENCEPHALOPATHIES

Abstract

Currently sepsis and liver failure are the most often reasons of the endogenous intoxication which causes damage of the brain and toxic encephalopathy. The sepsis-associated encephalopathy (SAE) can result in cognitive alterations up to coma. Acute hepatic encephalopathy (AHE) manifests also as acute cerebral dysfunction and usually occurs in severe form, accompanied by cytotoxic brain oedema. The mechanisms of SAE and AHE are to be elucidated, but the common links in their development are microglial activation and neuroinflammation [1]. In is considered that in case of systemic inflammation microglia transform to the neurotoxic phenotype and produce proinflammatory cytokines supporting uncontrolled neuroinflammation [2]. Given the identified morpho-functional heterogeneity of the microglia [3], more detailed research of the microglial activation in different brain regions would be useful for understanding mechanisms of the cerebral dysfunction in the conditions of sepsis and acute liver failure. The purpose of the study was analyzing immunohistochemical (IHC) specificity of the microglial reactivity in different brain regions in the conditions of experimental SAE and AHE. The study was conducted in Wistar rats, which were subjected to cecal ligation and puncture (CLP) model of sepsis and acetaminophen induced liver failure (AILF) model of AHE [1]. Microglial activation was determined by IHC evaluation of the expression of CD68 in the cortex, white matter, hippocampus, thalamus, caudate/putamen in the relative area (S rel., %) of CD68 + and