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Home » Archive » 2021

TDK conference 2021

In Vitro Examination of the Microglia-Independent Neuroinflammatory Role of Astrocytes in Hepatic Encephalopathy
Mónus Fanni Márta - year 6
University of Veterinary Medicine Budapest, Department of Physiology and Biochemistry
Supervisors: Dr. Zoltán Bárány, Dr. Dávid Sándor Kiss

Abstract:

Hepatic encephalopathy (HE) is a neurological disorder of multifactorial origin, caused by severe acute and chronic liver disease or portosystemic shunts. Impaired functions might be suspected in both cognitive and motor functions as well. The disorder has practical significance in aspects of both veterinary and human medicine.

Known as the main etiological factors of HE, hyperammonaemia, the accumulation of manganese and the oxidative stress have an impact on the function of microglia and astrocytes. These two types of support cells have a neuroprotective role in the central nervous system. As a neurotoxin, ammonia and manganese contributes to neuroinflammation which is an important process in the pathogenesis of HE. Astrocytes are responsible for the detoxification of certain toxins (e.g. ammonia) penetrating the blood-brain barrier. Previous research shows that microglia have a leading role in inducing inflammation, however astrocytes are also able to produce cytokines. Our aim in this research was the examination of astrocytes regarding their inflammatory role in the process of HE.

In our experiment we observed the production of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) using an in vitro model derived from pervious examinations at the department regarding the certain mechanisms of the pathogenesis of HE. Using the brain tissue of 1-2 days old Sprague-Dawly rats, we created a confluent astrocyte cell culture. To minimize the microglial cell-count a method based on shaking was applied. Different concentrations of agents contributing to HE was applied in our pure primary rat astrocyte-culture. Investigations were carried out to determine the effect on the production of TNF-α and IL-6 of hydrogen peroxide, ammonia, manganese and bacterial lipopolysaccharides.

Our results showed significant elevation of the examined cytokines in some aspects, however the effect of certain examined etiological agents of HE was not detectable in the means of cytokine production. Further investigations are necessary to understand the exact proinflammatory role of astrocytes in HE.



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