Objective To investigate the effects of dienogest on pain relief and inflammation in endometriosis (EMs), as well as its impact on the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) and nuclear factor kappa-B (NF-κB)/NOD-like receptor protein 3 (NLRP3) inflammatory pathways.
Methods An allograft method was used to establish an EMs rat model. The rats were randomly divided into sham-operated group (n=16), model group (n=16), low-dose dienogest group (n=16), medium-dose dienogest group (n=16) and high-dose dienogest group (n=16). After 7 days of treatment, the implantation volume and writhing response frequency were recorded. Enzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction and Western blotting were employed to measure the expression levels of vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α in the EMs rat models. Serum levels of BDNF, TrkB, NF-κB and NLRP3 were detected.
Results Compared with model group, dinorgestrel significantly reduced ectopic endometrial volume and torsion response of EMs (P < 0.05). Compared with model group, dinorgestrel significantly decreased the expression of VEGF, iNOS, IL6, IL-1β and TNF-α in EMs model (P < 0.05). In addition, compared with model group, dienogest significantly decreased the expressions of BDNF, TrkB, NF-κB and NLRP3 in ectopic endometrium (P < 0.05).
Conclusion Dinorgestrel can relieve EMS-related dysmenorrhea and inflammation, and its mechanism of action may be partly mediated by BDNF/TrkB pathway and NF-κB/NLRP3 pathway.
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