Cytotoxic Activity of the New Molecular Complex DHMEQ and Ammonium Glycyrrhizinate
- Authors
-
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Sh.R. Kzyrgalin
Department of Oncology and Clinical Morphology, Bashkir State Medical University, Ufa, Russian Federation and Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, Kazan, Russian Federation -
R.S. Yamidanov
Department of Oncology and Clinical Morphology, Bashkir State Medical University, Ufa, Russian Federation -
A.A. Rizvanov
Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, Kazan, Russian Federation and Division of Medical and Biological Sciences, Tatarstan Academy of Sciences, Kazan, Russian Federation -
Sh.Kh. Gantsev
Department of Oncology and Clinical Morphology, Bashkir State Medical University, Ufa, Russian Federation and Division of Medical Sciences and Healthcare, Academy of Sciences of the Republic of Bashkortostan, Ufa, Russian Federation
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- Keywords:
- Cytotoxicity, NF-κB inhibition, DHMEQ, ammonium glycyrrhizinate, molecular complex, transcription factor, in vitro, drug development
- Abstract
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Objective: This study aimed to investigate the cytotoxic activity of a new molecular complex consisting of DHMEQ and ammonium glycyrrhizinate, as well as its effect on the transcription factor NF-κB. Cytotoxicity was assessed using the PrestoBlue® viability assay in HEK293, A-549, and MCF-7 cell lines. NF-κB inhibition was evaluated via a luciferase reporter assay in HEK293 cells. The complex was prepared at a 1:4 molar ratio (DHMEQ:ammonium glycyrrhizinate), and its structure was confirmed using spectroscopic methods and electron microscopy. Statistical analysis was performed using one-way ANOVA followed by Dunnett’s post hoc test.
Results: DHMEQ demonstrated high cytotoxic activity (IC50 = 13.82 ± 3.71 µM in HEK293 cells). The DHMEQ/ammonium glycyrrhizinate complex maintained comparable activity (IC50 = 10.39 ± 1.84 µM for HEK293) but showed reduced efficacy against A-549 and MCF-7 tumor cells. DHMEQ strongly inhibited NF-κB activity (IC50 = 0.83 ± 0.51 µM), while the complex required significantly higher concentrations (IC50 = 21.79 ± 6.24 µM) to achieve a similar inhibitory effect.
Conclusion: The DHMEQ–ammonium glycyrrhizinate complex preserved the main biological properties of DHMEQ while improving its solubility and stability. This approach shows potential for developing DHMEQ-based drug formulations targeting NF-κB, but further optimization and in vivo validation are required before clinical application.
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- References
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- 16-09-2025
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- Vol. 14 (2025)
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