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Updated: Jun 26, 2026
Isolation of Primary Human Decidual Cells from the Fetal Membranes of Term Placentae
Published on: April 30, 2018
Liquiritin prevents preterm labor by remodeling decidual steroid homeostasis through 11β-HSD1 inhibition
Xiaowen Zhang1, Weishe Zhang1, Jingrui Huang1
1Department of Obstetrics, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Ethnopharmacological Relevance:
Licorice (Glycyrrhiza uralensis Fisch. ex DC.) is ethnobotanically indicated for stabilizing pregnancy and alleviating gestational abdominal pain. Its primary flavonoid, liquiritin (LQ), exhibits anti-inflammatory, antioxidant, and steroid-modulatory activities. Whether LQ prevents spontaneous preterm birth (sPTB) by rectifying placental inflammatory-metabolic imbalance remains unknown.
Aim Of The Study:
This study investigated the pharmacological efficacy of LQ against sPTB while deciphering the molecular mechanisms.
Materials And Methods:
The therapeutic efficacy of LQ was initially assessed in a lipopolysaccharide (LPS)-induced intrauterine inflammation (IUI) murine model, integrating histopathological, transcriptomic, and molecular profiling analyses. Subsequently, the molecular target of LQ was elucidated via DARTS-MS, molecular docking, CETSA-WB, and enzyme activity measurements in human decidual stromal cells (hDSCs). Target dependency was further validated through siRNA-mediated knockdown and overexpression rescue experiments. Finally, the downstream signaling mechanisms were dissected using complementary molecular analyses.
Results:
In the LPS-induced IUI murine model, LQ markedly prolonged gestation and enhanced neonatal survival. Mechanistically, LQ recalibrated glucocorticoid-redox homeostasis by suppressing NOX2 expression and activating the Nrf2/HO-1 antioxidant axis. In primary hDSCs, integrated chemoproteomics and biochemical assays identified 11β-HSD1 as a high-affinity functional target of LQ. Mechanistic interrogation confirmed that LQ-mediated 11β-HSD1 inhibition disrupts a pro-inflammatory loop, specifically suppressing cortisol amplification and subsequent COX-2/NOX2 cascades, which in turn reduced prostaglandin production.
Conclusion:
This study demonstrates that LQ alleviates placental dysfunction by suppressing glucocorticoid excess and the associated pro-inflammatory cascade and identifies 11β-HSD1 as a direct target of LQ in hDSCs, supporting its potential as a metabolic intervention targeting steroid homeostasis for sPTB prevention.
