Evaluation of the Neuroprotective Effect of Magnesium-Bis-(2-Aminoethanesulfonic)-Butanedioate in Simulated Ischemic Stroke in Rats

Sudden loss of blood flow to an area of the brain causes ischemic stroke, which leads to the loss of nerve function in the brain. The brain tissue leads to the death of brain cells in less than a few minutes due to the lack of oxygen and nutrients. This study aimed to evaluate the effectiveness of pharmacological correction of the consequences of ischemic stroke with a new derivative of taurine magnesium-bis-(2-aminoethanesulfonic)-butanedioate under laboratory code LKHT 3-17 in rats. The ischemic stroke was simulated by electrocoagulation of the right middle cerebral artery. The assessment of lethality, neurological status, locomotor, exploratory behavior, and morphological pattern of the brain damage was carried out on the 1st, 3rd, and 7th day after the pathology simulation. Neurological deficit 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, including the average thickness of the brain cortex and the number of neurons without degenerative changes. The substances were administered 60 minutes before the start of surgery. The animals were divided into an intact group (n=20); ischemic stroke simulation group without pharmacological correction (n=50); a group with correction of the ischemic stroke with taurine at the dose of 50 mg/kg (n=50); and a group with correction of ischemic stroke with magnesium-bis-(2-aminoethanesulfonic)-butadioate (LKHT 3-17) at the dose of 150 mg/kg (n=50).LHT 3-17 (150 mg/kg) and taurine (50 mg/kg) reduced lethality by 1.55 and 1.47 times, respectively, on the 7th day after stroke, compared to the control group (P<0.05). In parallel, an effective correction of neurological deficit was found for LKHT 3-17 and taurine to 4.0±0.8 and 7.6±0.9, respectively, on the 3rd day in contrast to the control of 8.1±0.8 points. The locomotor and exploratory behavior was most significantly different on the 1st and 7th days and was accompanied by a significant increase in the speed of movement under the influence of LKHT3-17 to 20 and 20 conventional units, compared to the control of 7 and 5 cu. On the 1st day, the thickness of the cortex was 1877.3±43.3 µm in the control group, and 1531.8±39.1 µm in the LKHT 3-17 group. The number of neurons without neurodegenerative changes prevailed in the group administered with LHT 3-17 (19.3±4.3), and the lowest number was observed in the group without pharmacological correction of the pathology (14.3±3.7).LKHT 3-17 at a dose of 150 mg/kg is more effective than taurine 50 mg/kg in protecting nerve activity in experimental ischemic stroke and reducing lethality, minimizing nerve defects, reducing volume, accelerating the process of tissue repair, helping stroke, and activating the regenerative processes.