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Jul 31, 2026Keywords:
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Main Article Content
Targeting endometriosis, preserving receptivity: Molecular insights into glycitein's selective action
Abstract
Methods: Molecular docking studies were conducted to determine the interaction between glycitein and specific receptors associated with the pathogenesis of endometriosis, such as estrogen receptor-α (ERα), estrogen receptor-β (ERβ), tumour necrosis factor-α (TNF-α), nuclear factor-κB (NF-κB), Prostaglandin EP3, and apoptosis proteins such as survivin, B-cell lymphoma 2 (BCL2), B-cell lymphoma-extra-large (BCL-XL), and Fas ligand (FASL). Binding properties of glycitein were compared with those of dienogest.
Results: Glycitein showed superior binding affinity to NF-κB receptor (-6.4 kcal/mol) and stronger interaction with prostaglandin EP3 receptor (-9.2 kcal/mol) compared to dienogest. In contrast, glycitein showed weaker binding affinity to apoptosis-regulating proteins, including survivin (-4.5 kcal/mol), BCL2 (-6.4 kcal/mol), BCL-XL (-6.7 kcal/mol), and FASL (-5.6 kcal/mol), compared to dienogest (-5.7, -7.6, -8.3, and -6.9 kcal/mol, respectively).
Conclusion: The computational study has shown that glycitein exerted potent anti-inflammatory activity by inhibiting the NF-κB pathway and prostaglandin EP3 receptor, but had minimal effects on endometrial apoptotic mediators. Such selectivity indicated that glycitein is likely to prevent endometriosis development without negatively affecting endometrial receptivity.
