Investigation of Taurine Derivative Magnesium-Bis-(2-Aminoethanesulfonic)-Butadioate on Alleviation of Neurological Defects in Simulated Hemorrhagic Stroke in Rats

Stroke or ischemia is caused by a partial or complete reduction in blood flow to the brain. Ischemia may be caused by cardiac arrest or by blockage of a specific blood vessel. Nutritional factors such as antioxidants and healthy eating patterns are important variables for stroke. Molecular composition properties, which include molecular binding and molecular screening, can be used to evaluate the specific activity and morphological changes. The aim of this study was to evaluate the effectiveness of pharmacological correction of the consequences of a hemorrhagic stroke with a new derivative of taurine magnesium-bis-(2-aminoethanesulfonic)-butadioate in rats. The animals (n=170) were divided into four groups as follows: 1) Control group (n=20); 2) Group 2 underwent the hemorrhagic stroke without pharmacological correction (n=50); 3) Group 3 (n=50) underwent simulation of hemorrhagic stroke received Taurine at the dose of 50 mg/kg; 4) Group 4 underwent simulation of hemorrhagic stroke with correction of hemorrhagic stroke with magnesium-bis-(2-aminoethanesulfonic)-butadioate at the dose of 150 mg/kg (LKHT 3-17 ) (n=50). A hemorrhagic stroke was induced by introducing autologous blood into the parietal lobe of the right hemisphere of the brain. The assessment of lethality, neurological status, locomotor, and exploratory behavior, and morphological pattern of the brain damage was carried out on the 1st, 3rd, and 7th days after the pathology simulation. Neurological deficit in animals was determined by the McGrow stroke index scale. The locomotor and exploratory behavior was evaluated using the Acti-track software and hardware complex. When assessing the morphological changes in the brain, attention was paid to two criteria: the average thickness of the brain cortex in microns and the number of neurons without degenerative changes. LKHT 3-17 (150 mg/kg) and taurine (50 mg/kg) reduced lethality by 1.7 and 1.36 times respectively on the 3rd day after stroke compared to the control (p<0.05). In parallel, an effective correction of neurological deficit was found for LKHT 3-17 and taurine to 5.3±0.8 and 6.5±0.9 respectively on the 1st day in contrast to the control of 8.1±0.7 points. The locomotor and exploratory behavior was most significantly different on the 7th day and was accompanied by a significant increase in total activity under the influence of LKHT 3-17 to 491 conventional units (cu) compared to the control of 110 conventional units. On the 1st day, the thickness of the cortex was 1943.7±44.08 µm in the control group, and 1491.0±38.61 µm in LKHT 3-17 group. The number of neurons without neurodegenerative changes prevailed in LKHT 3-17 group (18.7±4.32), and the lowest number was observed in the group without pharmacological correction of the pathology (14.3±3.78). The taurine derivative magnesium-bis-(2-aminoethanesulfonic)-butadioate, which is a combination of the amino acid, a magnesium ion, and succinic acid, decreases the neurological deficits, lethality, and enhances the locomotor and exploratory behavior in experimental hemorrhagic stroke in rats. The effect of the studied drug on the dynamics of molecular pathophysiological mechanisms occurring in the cell requires additional research.