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<p><b>Objective.</b> To compare the effects of Mexidol, Cerebrolysin, and Cortexin on the levels of brain-derived neurotrophic factor (BDNF), tumor necrosis factor alpha (TNF-α), and apoptosis markers in the rat brain during occlusion–reperfusion of the middle cerebral artery (MCA). <b>Materials and methods.</b> The study was performed on male Wistar rats. Right occlusion–reperfusion of the MCA was modeled as described by Koizumi (1986). The duration of occlusion was 60 min. At the onset of reperfusion, animals received a single i.v. injection of saline (control), i.v. Mexidol at a dose of 50 mg/kg, i.p. Cerebrolysin at a dose of 215 mg/kg, or i.p. Cortexin at a dose of 1 mg/kg. Brain lesion volume was analyzed 24 h after the onset of reperfusion after staining with 1% 2,3,5-triphenyltetrazolium solution. Levels of BDNF, TNF-α, and apoptosis markers Fas, bax, and caspase 3 in ischemic hemispheres were estimated by Western blotting. Five animals were included in each group for biochemical studies. <b>Results.</b> Modeling of occlusion–reperfusion of the MCA produced lesions in which necrosis volume in the affected hemisphere of the control animals was 38.16 ± 5.98%. Mexidol reduced necrosis volume to 20.48 ± 2.33% (<i>p</i> &lt; 0.001), Cerebrolysin to 32.57 ± 3.31% (<i>p</i> = 0.176), and Cortexin to 32.75 ± 4.91% (<i>p</i> = 0.198). Modeling of pathology provoked development of neuroinflammation, with an increase in TNF-α content, and activation of apoptosis, manifest as increases in Fas, bax, and caspase 3 levels, but had no effect on the BDNF level. Administration of Mexidol increased the BDNF level in the ischemic hemisphere and decreased Fas, bax, caspase 3, and TNF-α contents. Cerebrolysin had similar effects, albeit to a lesser extent. Cortexin did not affect the BDNF level but decreased TNF-α, Fas, and bax contents. <b>Conclusions.</b> Thus, when substances were given at the beginning of reperfusion after MCA occlusion, the most marked cerebroprotective effect was produced by Mexidol, which stimulates neurogenesis and suppresses the development of neuroinflammation and apoptosis.</p>

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The Effect of Neuroprotectors on BDNF, Tumor Necrosis Factor Alpha, and Apoptosis Marker Levels in Acute Cerebrovascular Accidents

  • 期刊论文

  • 发表日期：

    2026年8月3日

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  • A. V. Shchulkin,
  • I. V. Chernykh,
  • Yu. V. Abalenikhina,
  • M. V. Gatsanoga,
  • D. L. Kochetkova,
  • N. A. Kruzhalov,
  • E. V. Krestinina,
  • E. N. Yakusheva

摘要

Objective. To compare the effects of Mexidol, Cerebrolysin, and Cortexin on the levels of brain-derived neurotrophic factor (BDNF), tumor necrosis factor alpha (TNF-α), and apoptosis markers in the rat brain during occlusion–reperfusion of the middle cerebral artery (MCA). Materials and methods. The study was performed on male Wistar rats. Right occlusion–reperfusion of the MCA was modeled as described by Koizumi (1986). The duration of occlusion was 60 min. At the onset of reperfusion, animals received a single i.v. injection of saline (control), i.v. Mexidol at a dose of 50 mg/kg, i.p. Cerebrolysin at a dose of 215 mg/kg, or i.p. Cortexin at a dose of 1 mg/kg. Brain lesion volume was analyzed 24 h after the onset of reperfusion after staining with 1% 2,3,5-triphenyltetrazolium solution. Levels of BDNF, TNF-α, and apoptosis markers Fas, bax, and caspase 3 in ischemic hemispheres were estimated by Western blotting. Five animals were included in each group for biochemical studies. Results. Modeling of occlusion–reperfusion of the MCA produced lesions in which necrosis volume in the affected hemisphere of the control animals was 38.16 ± 5.98%. Mexidol reduced necrosis volume to 20.48 ± 2.33% (p < 0.001), Cerebrolysin to 32.57 ± 3.31% (p = 0.176), and Cortexin to 32.75 ± 4.91% (p = 0.198). Modeling of pathology provoked development of neuroinflammation, with an increase in TNF-α content, and activation of apoptosis, manifest as increases in Fas, bax, and caspase 3 levels, but had no effect on the BDNF level. Administration of Mexidol increased the BDNF level in the ischemic hemisphere and decreased Fas, bax, caspase 3, and TNF-α contents. Cerebrolysin had similar effects, albeit to a lesser extent. Cortexin did not affect the BDNF level but decreased TNF-α, Fas, and bax contents. Conclusions. Thus, when substances were given at the beginning of reperfusion after MCA occlusion, the most marked cerebroprotective effect was produced by Mexidol, which stimulates neurogenesis and suppresses the development of neuroinflammation and apoptosis.