Molecular Interactions of Genistein as a Potential Anti-Endometriosis

In: 2025 17th International Conference on Bioinformatics and Biomedical Technology (ICBBT) · 2025 · pp. 146–152 · doi:10.1109/icbbt65815.2025.11276401 · W4417339183
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This study investigated genistein's molecular interactions with endometriosis-related protein receptors, finding it binds strongly to Estrogen-$\beta$, Prostaglandin EP3, Estrogen-$\alpha$, TNF-$\alpha$, and NF-$\kappa$B receptors, primarily via hydrogen bonds.

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Abstract

Endometriosis is a gynecological disease that occurs in about 190 million women worldwide, with chronic pelvic pain, dysmenorhea and infertility as its main clinical manifestation. Current management targeting down-regulation of estrogen activity, has not shown satisfactory result due its side effect and reproductive function suppression. Genistein has well-researched, showing anti inflammation and antioxidant effects, that could potentially be used in the treatment of endometriosis. This study explore the interaction between genistein and protein receptors related to endometriosis pathogenesis. Genistein component were initially identified with their targeted protein receptors. The ligand and proteins were tested using Autodock program to predict possible binding sites between genistein and some target protein receptors associated with inflammatory activity in endometriosis models. Receptor modelling is then performed using Swiss-Model. Genistein showed strong binding potential toward Estrogen- $\beta$, Prostaglandin EP3, Estrogen- $\alpha$, TNF- $\alpha$, and $\text{NF}-\kappa \mathrm{B}$ protein receptors respectively. Genistein mostly bind with hydrogen bond with the target protein receptors. Genistein has the ability to interconnected with receptors related to reproductive function and inflammatory processes, a significant factor associated with the pathogenesis of endometriosis.

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Condition tags

endometriosischronic_pelvic_paininfertility

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (30)

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