Reactive astrogliosis in rats with LPS-induced Parkinson's disease

Zh. Oliynyk, N. Senchylo, T. Dovbynchuk, S. Stepanenko, M. Guzik
Taras Shevchenko National University of Kyiv, Kyiv; Taras Shevchenko National University of Kyiv, Kyiv; Taras Shevchenko National University of Kyiv, Kyiv; Taras Shevchenko National University of Kyiv, Kyiv; Palladin Institute of Biochemistry of the National Academy of Sciences of Ukraine (NASU)


The astrogliosis was considered as a beneficial process to protect neurons and repair the tissue after CNS insult for a long time. However,
numerous study indicate that under some specific conditions, reactive astrocytes can exacerbate neuroinflammation and tissue damage.
Parkinson's disease (PD) is one of the most common neurodegenerative diseases that is a major medical and social problem. The progressive course of the disease requires continuous therapy, in the later stages it causes a disability of the patient, which entails the need for constant care and causes significant economic losses. The pathophysiological bases of CP remain unclear, making it impossible to diagnose the disease early, predict its course, and develop pathogenetic treatments. Neuroinflammation of polyetiological genesis, whose development involves micro- and astroglial cells, is considered to be a leading pathogenetic factor of CP. However, the functional state of astroglia in the conditions of development of this neuropathology remains the least studied. The aim of the study was to investigate the functional state of astroglia in rats with PD induced by bacterial lipopolysaccharide (LPS-PD). It has been established that the development of LPS-PD in rats is accompanied by reactive astrogliosis with overexpression of glial fibrillar acidic protein (GFAP) and products of its degradation by astrocytes of the hippocampal region of the brain.
Overexpression of GFAP is associated with an increase in the level of myelin basic protein (MBP) in brain homogenates and a decrease in the level of neuronal NO synthase.


Parkinson's disease, astrogliosis, glial fibrillary acidic protein, myelin basic protein, neuronal NO synthase

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Received: 17.01.2020

Revised: 17.02.2020

Signed for the press: 17.02.2020



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