The effect of Mexidol on the level of neurogenesis markers in acute cerebrovascular disorders in the experiment

Authors:

A.V. Schulkin, I.V. Chernykh, Yu.V. Abalenikhina, M.V. Gatsanoga, O.A. Andryushin, N.A. Kruzhalov, E.N. Yakusheva

FGBOU in the Ryazan State Medical University named after Academician I.P. Pavlova "of the Ministry of Health of Russia, Ryazan, Russia

Place of publication:

S.S. Korsakov Journal of Neurology and Psychiatry
2025, Vol. 125, No. 2, pp. 107–112

The aim of the study was to examine the effect of Mexidol on the levels of factors regulating neurogenesis.

Material and methods. The study was performed on male Wistar rats. Focal cerebral ischemia was reproduced by endovascular occlusion-reperfusion of the right middle cerebral artery according to the method of J. Koizumi (1986). The duration of occlusion was 60 min. At the onset of reperfusion, the animals received a single intravenous injection of saline or Mexidol at a dose of 50 mg/kg. At 4 h, 8 h, and 24 h after the onset of reperfusion, the relative amount of molecules regulating neurogenesis in the ischemic hemisphere was assessed by Western blot. Additionally, 24 h after the onset of reperfusion, the size of the cerebral infarction was analyzed after staining with a 1% solution of 2,3,5,-triphenyltetrazolium.

Results. In a model of middle cerebral artery occlusion-reperfusion, the volume of necrosis in the affected hemisphere of animals administered saline was 37.75±7.46%, while the administration of Mexidol at a dose of 50 mg/kg led to a decrease in the necrosis volume to 20.48±2.33% (p=0.0006). Modeling of middle cerebral artery occlusion-reperfusion was accompanied by activation of the neurotrophic factors IGF-1, NGF, and the vascular growth factor VEGF. A single intravenous administration of Mexidol at a dose of 50 mg/kg during reperfusion was accompanied by a more significant increase
in the level of neurotrophic factors IGF-1, NGF, BDNF and VEGF in the ischemic area of ​​the brain compared to the administration of saline, which leads to increased neuroregeneration at all observation times (4 hours, 8 hours and 24 hours after reperfusion), the marker of which is tubulin-3.

Conclusion. The obtained results indicate that Mexidol not only has a protective effect on neurons but can also stimulate neuroregeneration by increasing the levels of key regulatory molecules.

Key words: Mexidol, ethylmethylhydroxypyridine succinate, acute cerebrovascular accident, neurogenesis, blood-brain barrier.