Journal of ethnopharmacology · 2026
Integrated serum pharmacochemistry , network pharmacology, untargeted metabolomics and experimental validation to explore the mechanism of Wenjian Qigong Decoction in the treatment of polycystic ovary syndrome.
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Wang Xinbo, Liu Chuyi, Zhang Zhuo, Huang Yanjing, Liu Zhuo, Song Yufan, Hu Runan, Ma Wenwen, Song Kunkun, Zhang Mingmin, Dong Haoxu
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Polycystic ovary syndrome (PCOS), a prevalent endocrine and metabolic disorder among women of reproductive age, currently has no definitive treatment. Qigong Wan (QGW), first documented in Yifang Jijie, is a classic prescription for infertility in obese women. Given the heterogeneous and complex nature of PCOS, Wenjian Qigong Decoction (WJQG), a modified formula derived from QGW that incorporates medicinal ingredients from Jiawei Buzhong Yiqi Decoction (JWBZYQ), Guishen Wan (GSW), and Jiaotai Wan (JTW), exhibits remarkable therapeutic efficacy for obese PCOS in clinical practice. The efficacy of all constituent herbs in WJQG has been confirmed, whereas its pharmacological mechanisms remain to be clarified.
AIM OF THE STUDY: To investigate the potential therapeutic benefits of WJQG for the treatment of PCOS and provide mechanistic insights into its mode of action.
MATERIALS AND METHODS: An obese PCOS rat model was established via testosterone propionate (TP) injection combined with a 45% high-fat diet (HFD). The therapeutic efficacy of WJQG, as well as the validity of the model, was evaluated by assessing body weight, visceral fat content, estrous cycle, clinical chemistry indicators, and histopathology. Furthermore, a comprehensive approach integrating ovarian untargeted metabolomics, serum pharmacochemistry , network pharmacology, molecular docking, and experimental validation was employed to systematically elucidate the potential mechanism of action of WJQG in treating obese PCOS.
RESULTS: WJQG significantly attenuated body weight gain, reduced abdominal visceral fat, restored estrous cyclicity, improved ovarian morphology, and corrected hyperandrogenemia and endocrine dysregulation in obese PCOS rats. Serum pharmacochemistry identified 22 bioactive prototype compounds absorbed into the blood. Network pharmacology predicted hub targets including TNF, IL6, CASP3, and PTGS2. Subsequent molecular docking simulations indicated favorable binding affinities between these proteins and representative prototype constituents such as narirutin, ginsenoside Rc, and hyperoside. Untargeted metabolomics suggested that WJQG substantially remodeled the ovarian metabolome, specifically suppressing the hyperactivated arachidonic acid metabolism pathway and downregulating downstream pro-inflammatory lipid mediators (PGF2α, PGA2, PGE2, and 10,11-dihydro-20-hydroxy-LTB4). Mechanistically, WJQG inhibited the enzymatic cascade of p-cPLA2, COX-2 (encoded by PTGS2), and 5-LOX. Meanwhile, WJQG treatment was associated with restored ADPN/PPARα/p-AMPK signaling, a predominance of M2-type macrophages, a suppressed NLRP3/NF-κB inflammatory cascade accompanied by reduced TNF-α and IL-6 levels, and alleviated granulosa-cell apoptosis alongside decreased caspase-3 activation.
CONCLUSIONS: WJQG alleviates key disease manifestations in obese PCOS rats, which correlates with modulation of the interconnected pathological triad of intra-ovarian arachidonic acid metabolism hyperactivation, chronic inflammation, and granulosa-cell apoptosis. These findings provide supportive scientific evidence and pharmacodynamic rationale to support further pre-clinical investigation of WJQG as a potential integrative therapeutic candidate for PCOS.
AIM OF THE STUDY: To investigate the potential therapeutic benefits of WJQG for the treatment of PCOS and provide mechanistic insights into its mode of action.
MATERIALS AND METHODS: An obese PCOS rat model was established via testosterone propionate (TP) injection combined with a 45% high-fat diet (HFD). The therapeutic efficacy of WJQG, as well as the validity of the model, was evaluated by assessing body weight, visceral fat content, estrous cycle, clinical chemistry indicators, and histopathology. Furthermore, a comprehensive approach integrating ovarian untargeted metabolomics, serum pharmacochemistry , network pharmacology, molecular docking, and experimental validation was employed to systematically elucidate the potential mechanism of action of WJQG in treating obese PCOS.
RESULTS: WJQG significantly attenuated body weight gain, reduced abdominal visceral fat, restored estrous cyclicity, improved ovarian morphology, and corrected hyperandrogenemia and endocrine dysregulation in obese PCOS rats. Serum pharmacochemistry identified 22 bioactive prototype compounds absorbed into the blood. Network pharmacology predicted hub targets including TNF, IL6, CASP3, and PTGS2. Subsequent molecular docking simulations indicated favorable binding affinities between these proteins and representative prototype constituents such as narirutin, ginsenoside Rc, and hyperoside. Untargeted metabolomics suggested that WJQG substantially remodeled the ovarian metabolome, specifically suppressing the hyperactivated arachidonic acid metabolism pathway and downregulating downstream pro-inflammatory lipid mediators (PGF2α, PGA2, PGE2, and 10,11-dihydro-20-hydroxy-LTB4). Mechanistically, WJQG inhibited the enzymatic cascade of p-cPLA2, COX-2 (encoded by PTGS2), and 5-LOX. Meanwhile, WJQG treatment was associated with restored ADPN/PPARα/p-AMPK signaling, a predominance of M2-type macrophages, a suppressed NLRP3/NF-κB inflammatory cascade accompanied by reduced TNF-α and IL-6 levels, and alleviated granulosa-cell apoptosis alongside decreased caspase-3 activation.
CONCLUSIONS: WJQG alleviates key disease manifestations in obese PCOS rats, which correlates with modulation of the interconnected pathological triad of intra-ovarian arachidonic acid metabolism hyperactivation, chronic inflammation, and granulosa-cell apoptosis. These findings provide supportive scientific evidence and pharmacodynamic rationale to support further pre-clinical investigation of WJQG as a potential integrative therapeutic candidate for PCOS.