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J Herbmed Pharmacol. 2024;13(1): 137-143.
doi: 10.34172/jhp.2024.48225
  Abstract View: 147
  PDF Download: 104

Original Article

Effect of pinocembrin on thymocyte proliferation and death

Gulnoza Toshtemirova 1 ORCID logo, Sarvinoz Rustamova 1 ORCID logo, Nargiza Tsiferova 1, 2 ORCID logo, Galina Maksimcheva 1, 2 ORCID logo, Petr Merzlyak 1 ORCID logo, Ranohon Kurbannazarova 1, 3 ORCID logo, Ravshan Sabirov 1, 3* ORCID logo

1 Institute of Biophysics and Biochemistry, National University of Uzbekistan, Tashkent, Uzbekistan
2 Center for Advanced Technologies, Ministry of Higher Education, Science and Innovation of the Republic of Uzbekistan
3 Department of Biophysics, National University of Uzbekistan, Tashkent, Uzbekistan
*Corresponding Author: *Corresponding author: Ravshan Sabirov, Email: , Email: zairovich@gmail.com

Abstract

Introduction: Cell volume regulation is critical for cellular proliferation and death. Pinocembrin effectively suppresses the volume regulation in thymocytes under hypoosmotic stress by blocking the volume-sensitive anion channel. This study aims to evaluate the effects of this flavonoid on thymocyte proliferation and death.

Methods: Thymocytes were cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum, and the cell number was determined by cloud-based automated cell counting (Corning). Necrotic and apoptotic cell death were evaluated by propidium iodide- and annexin V-staining, respectively.

Results: Pinocembrin at 10–50 μM caused suppression of primary cultured thymocyte proliferation with a half-maximal effect of 28.4 ± 0.2 μM. The cell counts did not fall below the control level at the doses of 100–150 μM. The fraction of spontaneously necrotic cells was ~26% of the total population and increased to ~51% in the presence of dexamethasone. The fraction of spontaneously apoptotic cells increased by this glucocorticoid from 3.6% to 16.7%. Pinocembrin protected thymocytes from necrosis both in spontaneous and dexamethasone-induced death, reducing the fraction of necrotic cells by ~40–50% at 150 μM. Pinocembrin attenuated dexamethasone-induced apoptotic death, reducing the fraction of annexin-positive cells to the control (spontaneous) level.

Conclusion: Our results suggest that pinocembrin arrests thymocyte proliferation without essential killing. Under conditions of massive death (e.g., during inflammation, when the level of glucocorticoids increases sharply both physiologically and as a result of pharmacotherapy), pinocembrin protects immuno-competent cells from necrotic and apoptotic death.


Implication for health policy/practice/research/medical education:

This paper provides experimental evidence of the antiproliferative activity of pinocembrin on thymocytes and the protection of cells against necrotic and apoptotic death, both spontaneous and glucocorticoid-induced. These results have implications for the pharmacodynamics of pinocembrin and therapeutic strategies when using pinocembrin-based pharmaceuticals.

Please cite this paper as: Toshtemirova G, Rustamova S, Tsiferova N, Maksimcheva G, Kurbannazarova R, Merzlyak P, et al. Effect of pinocembrin on thymocyte proliferation and death. J Herbmed Pharmacol. 2024;13(1):137-143. doi: 10.34172/ jhp.2024.48225.

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Submitted: 21 Jun 2023
Revision: 06 Oct 2023
Accepted: 14 Oct 2023
ePublished: 01 Jan 2024
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