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Heat Shock Protein HSP27 and the Status of the Glutathione System in Dexamethasone-Induced Apoptosis of Jurkat Tumor Cells

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We studied the effect of the HSP27 inhibitor, 5-(5-ethyl-2-hydroxy-4-methoxyphenyl)-4-(4-methoxyphenyl)-isoxazole, at a final concentration of 0.1 μM and/or the apoptosis inducer dexamethasone at a final concentration of 10 μM on the content of hydroxyl radical, reduced and oxidized glutathione, HSP27, activity of glutathione reductase, glutathione peroxidase, caspase-3, and the number of Annexin+ Jurkat tumor cells. The involvement of HSP27 in apoptosis of Jurkat tumor cells was demonstrated. Simultaneous exposure to the HSP27 inhibitor and dexamethasone resulted in an increase in the level of HSP27 against the background of developing oxidative stress (increase in the concentration of hydroxyl radicals and changes in the state of the glutathione system).

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Authors and Affiliations

  1. Siberian State Medical University, Ministry of Health of the Russian Federation, Tomsk, Russia

    O. L. Nosareva & E. A. Stepovaya

  2. Immanuel Kant Baltic Federal University, Kaliningrad, Russia

    L. S. Litvinova & K. A. Yurova

Authors
  1. O. L. Nosareva
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  2. E. A. Stepovaya
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  3. L. S. Litvinova
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  4. K. A. Yurova
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Corresponding author

Correspondence to O. L. Nosareva.

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Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 176, No. 11, pp. 638-640, November, 2023

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Nosareva, O.L., Stepovaya, E.A., Litvinova, L.S. et al. Heat Shock Protein HSP27 and the Status of the Glutathione System in Dexamethasone-Induced Apoptosis of Jurkat Tumor Cells. Bull Exp Biol Med 176, 617–619 (2024). https://doi.org/10.1007/s10517-024-06079-y

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  • DOI: https://doi.org/10.1007/s10517-024-06079-y

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