Abstract <p>In this study, we evaluated the possibility of potentiatingthe neurorehabilitation effect of hypercapnic hypoxia (HyperH) bythe JNK (c-Jun-N-terminal kinase) inhibitor IQ-1 (11<i>H</i>-indeno[1,2-<i>b</i>]quinoxalin-11-oneoxime) after photochemically induced cerebral thrombosis in rats.Forty male Wistar rats were divided into 4 equal groups (<i>n</i> = 10), which underwent a courseof respiratory HyperH exposures for 30 min a day, 15 sessions: (1)HyperH group (P<sub>O2</sub> ≈ 90 mm Hg, P<sub>CO2</sub> ≈50 mm Hg); (2)&#xa0;HyperH + IQ-1 group; (3) Con (control) group; (4)Soc (sham-operated control) comparison group. After completion ofthe rehabilitation course, HyperH-exposed animals showed a two-foldreduction in infarct volume compared to the Con group, and an improvementin motor-coordination functions. Combining HyperH with IQ-1 administration enhancedHyperH efficacy only in terms of restoring motor functions (assessedin the rotarod test) and reducing the serum concentration of neuron-specific enolase(NSE). The obtained data indicate that isolated HyperH exposureexerts a pronounced neurorehabilitation effect after focal ischemicinjury (<i>p</i> &lt; 0.05). However,combining respiratory training with the JNK blocker IQ-1 shows onlya partial potential for enhancing the neurorehabilitation effectof HyperH, which may be due to the delayed blocker administration.</p>

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JNK Inhibition Potentiates Neurorehabilitative Outcomes Induced by Hypercapnic Hypoxia

  • P. A. Chekulaev,
  • G. M. Zembatov,
  • E. D. Namiot,
  • M. A. Ignatyuk,
  • A. K. Berdnikov,
  • A. R. Kovrizhina,
  • V. P. Kulikov,
  • P. P. Tregub

摘要

Abstract

In this study, we evaluated the possibility of potentiatingthe neurorehabilitation effect of hypercapnic hypoxia (HyperH) bythe JNK (c-Jun-N-terminal kinase) inhibitor IQ-1 (11H-indeno[1,2-b]quinoxalin-11-oneoxime) after photochemically induced cerebral thrombosis in rats.Forty male Wistar rats were divided into 4 equal groups (n = 10), which underwent a courseof respiratory HyperH exposures for 30 min a day, 15 sessions: (1)HyperH group (PO2 ≈ 90 mm Hg, PCO2 ≈50 mm Hg); (2) HyperH + IQ-1 group; (3) Con (control) group; (4)Soc (sham-operated control) comparison group. After completion ofthe rehabilitation course, HyperH-exposed animals showed a two-foldreduction in infarct volume compared to the Con group, and an improvementin motor-coordination functions. Combining HyperH with IQ-1 administration enhancedHyperH efficacy only in terms of restoring motor functions (assessedin the rotarod test) and reducing the serum concentration of neuron-specific enolase(NSE). The obtained data indicate that isolated HyperH exposureexerts a pronounced neurorehabilitation effect after focal ischemicinjury (p < 0.05). However,combining respiratory training with the JNK blocker IQ-1 shows onlya partial potential for enhancing the neurorehabilitation effectof HyperH, which may be due to the delayed blocker administration.