Mild Moxibustion Alleviates Primary Dysmenorrhea in Rats Through TRPV1-Associated Modulation of NF-κB Signaling and Uterine Oxidative Stress

Abstract

Purpose To investigate the therapeutic effect and analgesic mechanism of mild moxibustion at Shenque (CV8) and Guanyuan (CV4) in a primary dysmenorrhea (PD) rat model, focusing on the involvement of TRPV1-NF-κB signaling and uterine oxidative stress. Methods Forty female Sprague-Dawley (SD) rats were randomly divided into five groups (n=8): blank group (BG), model group (MG), mild moxibustion group (MMG), antagonist capsazepine group (CPZG), and ibuprofen group (IG). PD models were established through cold stimulation combined with estradiol benzoate and oxytocin injection. The MMG received mild moxibustion at “Shenque” (CV8) and “Guanyuan” (CV4) acupoints. The CPZG was pretreated with capsazepine (CPZ) before moxibustion. The IG received ibuprofen via gavage. After intervention, pain thresholds and writhing scores were measured; uterine pathology was observed via HE staining; ELISA, colorimetric assay, immunohistochemistry (IHC), and Western blotting were used to detect relevant biomarkers. Results Mild moxibustion significantly elevated pain thresholds and reduced writhing scores (vs MG, P<0.01). Capsazepine partially reversed these analgesic effects (vs MMG, P<0.01). Mild moxibustion decreased serum IL-1β, TNF-α, and PGF2α while increasing PGE2 (vs MG, P<0.01). Mild moxibustion upregulated TRPV1 expression at acupoints (vs MG, P<0.01), whereas capsazepine suppressed TRPV1 expression (vs MMG, P<0.01). Mild moxibustion downregulated uterine NF-κB P-p65 and COX-2 expression (vs MG, P<0.01), while CPZG upregulated these proteins (vs MMG, P<0.01). Furthermore, mild moxibustion upregulated uterine SOD2 expression (vs MG, P<0.05), decreased MDA content, and increased GSH content and SOD activity (vs MG, P<0.05 or P<0.01). Conclusion Mild moxibustion at CV8 and CV4 alleviates PD in rats through mechanisms involving TRPV1 activation, NF-κB pathway modulation, and improvement of uterine oxidative stress. These findings provide a preclinical basis for further investigation.