Journal of ethnopharmacology · 2026
Taohe Chengqi Decoction ameliorates APID-related local uterine inflammatory injury through modulation of inflammation, oxidative stress, and JNK/p38 MAPK-NF-κB-related signaling.
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Wang Yi-Han, Wang Yan-Chen, Yuan Yi-Fan, Zhang Zi-Jian, Yan Xing-Tong, He Yan, Peng Liang, Zhang Gang, Gao Jing, Liu Ji-Ping, Yan Yong-Gang, Wang Hong-Yan
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Taohe Chengqi Decoction (THCQD), a classical formula from Shang Han Lun, is traditionally used to clear heat, purge accumulation, activate blood circulation, and dispel blood stasis in lower-jiao blood accumulation and gynecological stasis-heat disorders. Acute pelvic inflammatory disease (APID) frequently affects the upper female reproductive tract during reproductive age, and its acute-stage uterine injury is closely linked to inflammatory imbalance, oxidative stress, and local tissue damage. Therefore, evaluating THCQD in an experimental model of APID-related uterine inflammatory injury may provide evidence for its potential relevance to gynecological inflammatory injury.
AIM OF THE STUDY: To evaluate the effects of THCQD in a mechanical-chemical injury-induced rat model of APID-related local uterine inflammatory injury and to explore its possible association with inflammatory responses, oxidative stress, and JNK/p38 MAPK-NF-κB-apoptosis-related signaling.
MATERIALS AND METHODS: A rat model was generated using endometrial mechanical injury together with intrauterine injection of phenol mucilage. Pharmacodynamic effects and potential mechanisms were assessed by biochemical assays, ELISA, histopathology, UPLC-MS/MS profiling, network pharmacology, transcriptomics, molecular docking, Western blotting, RT-qPCR, and immunohistochemistry. Cell-based validation was performed using LPS-stimulated primary rat uterine endometrial epithelial cells, H-THCQD-containing serum, and JNK/p38 MAPK inhibitors.
RESULTS: THCQD improved inflammatory activation, redox imbalance, peripheral blood inflammatory cell abnormalities, and uterine pathological injury. Integrated analyses and experimental validation supported the possible involvement of JNK/p38 MAPK-NF-κB-apoptosis-related signaling in THCQD intervention.
CONCLUSION: THCQD alleviated APID-related local uterine inflammatory injury, and this effect may be associated with the involvement of JNK/p38 MAPK-NF-κB-apoptosis-related signaling. These findings provide experimental evidence for the effects of THCQD on APID-related uterine inflammatory injury and support further mechanistic research on classical formulas in gynecological inflammatory injury.
AIM OF THE STUDY: To evaluate the effects of THCQD in a mechanical-chemical injury-induced rat model of APID-related local uterine inflammatory injury and to explore its possible association with inflammatory responses, oxidative stress, and JNK/p38 MAPK-NF-κB-apoptosis-related signaling.
MATERIALS AND METHODS: A rat model was generated using endometrial mechanical injury together with intrauterine injection of phenol mucilage. Pharmacodynamic effects and potential mechanisms were assessed by biochemical assays, ELISA, histopathology, UPLC-MS/MS profiling, network pharmacology, transcriptomics, molecular docking, Western blotting, RT-qPCR, and immunohistochemistry. Cell-based validation was performed using LPS-stimulated primary rat uterine endometrial epithelial cells, H-THCQD-containing serum, and JNK/p38 MAPK inhibitors.
RESULTS: THCQD improved inflammatory activation, redox imbalance, peripheral blood inflammatory cell abnormalities, and uterine pathological injury. Integrated analyses and experimental validation supported the possible involvement of JNK/p38 MAPK-NF-κB-apoptosis-related signaling in THCQD intervention.
CONCLUSION: THCQD alleviated APID-related local uterine inflammatory injury, and this effect may be associated with the involvement of JNK/p38 MAPK-NF-κB-apoptosis-related signaling. These findings provide experimental evidence for the effects of THCQD on APID-related uterine inflammatory injury and support further mechanistic research on classical formulas in gynecological inflammatory injury.