Tag Archives: glial fibrillary acidic protein (GFAP)

Citicoline affects serum angiostatin and neurospecific protein levels in patients with atrial fibrillation and ischemic stroke

A. A. Tykhomyrov1, Yu. S. Kushnir2, V. S. Nedzvetsky3,
T. V. Grinenko1, O. V. Kuryata2

1Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
2State Establishment “Dnipropetrovsk Medical Academy of Health Ministry of Ukraine”, Dnipro;
3Bingöl University, Bingöl, Turkey;
e-mail: artem_tykhomyrov@ukr.net

Received: 22 May 2019; Accepted: 13 August 2019

Ischemic stroke is considered as one of the most frequent and severe complications of atrial fibrillation. The present study was undertaken to examine whether post-insult treatment with cytidine diphosphate-choline (CDP-choline, or citicoline) affects serum levels of the angiogenesis inhibitor angiostatin and neurospecific proteins as markers of brain damage in patients with cerebral ischemia associated with atrial fibrillation. Thirty-three patients with a diagnosis of acute ischemic stroke received citicoline sodium by intravenous infusions (1,000 mg daily for 14 days) in addition to the standard treatment (basic group). Twenty-five patients with the same pathologies, who received only standard therapy, were enrolled in the study as a control group. Serum content of angiostatin and neurospecific proteins, namely neurofilament heavy subunit (NF-H) and glial fibrillary acidic protein (GFAP), was measured by immunoblotting at the basal level and after the treatment. Citicoline treatment caused significant decreases in serum levels of angiostatin (by 40% vs. basal level, P < 0.05), GFAP (by 61%, P < 0.01), and the NF-H subunit (by 19%, P < 0.05) and had no effect on the serum albumin content. In contrast, there were no statistically significant differences between baseline levels of the studied protein markers and their content after the treatment period in the control group. These findings indicate for the first time that CDP-choline protects both astrocytes and neurons and improves angiogenic capacity through down-regulation of angiostatin in post-ischemic patients with atrial fibrillation after acute ischemic stroke. Further studies are needed to test associations between serum levels of these biomarkers, clinical outcomes, and treatment efficacy of stroke.

High thiamine dose restores levels of specific astroglial proteins in rat brain astrocytes affected by chronic ethanol consumption

O. S. Pavlova, A. A. Tykhomyrov, O. A. Mejenskaya,
S. P. Stepanenko, L. I. Chehivska, Yu. M. Parkhomenko

Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
e-mail: aspavlova92@gmail.com

Received: 23 January 2019; Accepted: 17 May 2019

Long-term ethyl alcohol consumption induces a deficiency of essential nutrient thiamine (vitamin B1 ) and profoundly impairs metabolic processes in nervous tissue, resulting in structural and functional alterations in the central nervous system (CNS). This study was performed to evaluate protective effects of thiamine acute dose on the level of glial fibrillary acidic protein (GFAP), a sensitive marker of astroglia, and B1-related enzyme thiamine pyrophosphokinase (TPK) activity in brain of rats chronically exposed to ethanol. The rats were divided into three groups as follows: i) control group; ii) rats given 15% ethanol solution as drinking water for 9 months (EtOH group), iii) EtOH rats given thiamine per os in a dose of 2.0 mg/kg one day before experiment termination (n = 4 in each group). GFAP levels were analyzed in cerebellum, brain cortex and hippocampus by western blot and immunohistochemistry. Brain TPK activity was measured with the use of the yeast apopyruvate decarboxylase apoenzyme (apoPDC). Thiamine concentration in liver was estimated with the use of thiochrome method. It was demonstrated that GFAP content was dramatically reduced in all studied brain regions of EtOH-exposed rats (approximately by 60%, P < 0.05) compared with control rats indica­ting profound astroglial dysfunction. Thiamine treatment was shown to recover GFAP levels up to 80% vs. control value in the brain of EtOH-exposed rats (P < 0.05). Ethanol consumption resulted in 3.7-fold decrease in liver thiamine content and 1.4-fold decrease in brain TPK activity, as compared with control (P < 0.05). Thiamine treatment of EtOH-exposed rats significantly elevated B1 liver level, however, had no effect on brain TPK activity. Our data suggest that thiamine deficit can play an important role in alcohol-induced damage to brain astroglia. It is emerged that high-dose thiamine administration can represent effective treatment option against chronic effects of ethanol impact on brain structures.