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Updated: Jul 14, 2026
Herbs-Partitioned Moxibustion on the Navel in a Rat Model of Primary Dysmenorrhea with Cold Coagulation and Blood Stasis
Published on: October 4, 2024
Ge-Gen Decoction Modulates the HSP90/AKT Signaling Pathway and the NLRP3 Inflammasome to Alleviate Primary
Yazhen Xie1, Limei Xu2, Yijuan He3
1Department of Gynaecology, Taicang Hospital of Traditional Chinese Medicine, Taicang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Taicang, Jiangsu, People's Republic of China.
Objective:
Ge-Gen Decoction (GGD) is a traditional Chinese medicinal formula composed of seven herbs (including Pueraria lobata, Ephedra sinica, and Cinnamomum cassia), commonly used for the treatment of primary dysmenorrhea (PDM). However, its mechanism is unclear. This animal study investigated whether GGD alleviates cold-damp stagnation-type PDM by modulating the HSP90/AKT signaling pathway and NLRP3 inflammasome.
Methods:
Female Wistar rats were subjected to cold stimulation plus estradiol benzoate and oxytocin to establish a PDM model. Rats were divided into five groups (n = 6 each): control, PDM model, GGD (1.8 g/kg), GGD plus Terazosin (an HSP90 agonist, 0.08 g/kg), and ibuprofen (0.06 g/kg). Treatments were given orally once daily. PDM severity was assessed by writhing frequency and latency. Uterine histopathology, serum prostaglandins (PGE2, PGF2α) and inflammatory cytokines (IL-1β, IL-18, IL-6) were measured. Uterine expression of HSP90, p-AKT, NLRP3, Caspase-1, and IL-1β was examined by immunohistochemistry.
Results:
Compared to controls, the model group showed increased writhing frequency, elevated PGF2α and PGF2α/PGE2 ratio, severe uterine damage, and upregulation of HSP90, p-AKT, NLRP3, Caspase-1, and IL-1β. GGD treatment significantly attenuated all these changes, with effects comparable to ibuprofen. Notably, co-administration of Terazosin (HSP90 inhibitor) reversed the protective effects of GGD. GGD also reduced serum IL-1β, IL-18, and IL-6, and this suppression was antagonized by Terazosin.
Conclusion:
GGD alleviates cold-damp stagnation-type PDM in a rat model. The findings suggest that its mechanism involves modulation of the HSP90/AKT pathway, thereby suppressing NLRP3 inflammasome activation and subsequent pro-inflammatory cytokine release.
