Combined Auricular Electrostimulation and Sunshi Dingtong Decoction Alleviate Primary Dysmenorrhea in Rats

Primary dysmenorrhea, characterized by severe lower abdominal pain, is a common gynecological disorder often linked to uterine inflammation and a qi stagnation and blood stasis pattern in traditional Chinese medicine. Current pharmacologic treatments, such as NSAIDs, can have adverse side effects, necessitating alternative therapies. This study explores the synergistic potential of auricular electrostimulation and a traditional herbal decoction to address the inflammatory and pathological hallmarks of this condition, specifically targeting the underlying molecular pathways.

Researchers induced a qi stagnation and blood stasis primary dysmenorrhea (QSBSPD) model in 36 female Sprague-Dawley rats using estradiol benzoate sensitization, epinephrine hydrochloride stress, and oxytocin. Rats were divided into blank, model, SDD, TEAP, TEAP plus SDD, and ibuprofen groups. Treatments involved normal saline, SDD, ibuprofen, or TEAP applied at defined auricular points for seven days. Uterine morphology was assessed via hematoxylin and eosin staining. Inflammatory markers IL-1β, IL-6, TNF-α, PGF2α, and PGE2 were quantified by ELISA, while PPAR-γ2 and COX-2 mRNA expression were measured using real-time PCR.

Model rats exhibited significant uterine epithelial degeneration and neutrophil infiltration. They also showed increased uterine levels of IL-1β, IL-6, TNF-α, PGF2α, and COX-2 mRNA expression, alongside decreased PGE2 and PPAR-γ2 mRNA expression. Treatment with TEAP or SDD alone partially reversed these pathological and molecular changes. However, the combined TEAP plus SDD intervention yielded more pronounced improvements across all measured parameters. > The combined TEAP plus SDD treatment produced effects comparable to those observed in the ibuprofen group, significantly alleviating uterine pathological injury and inflammation-related changes. These beneficial effects were specifically associated with the regulation of PPAR-γ2 and COX-2 mRNA expression, indicating a targeted anti-inflammatory mechanism.