Suppression of TLR4-MyD88 signaling pathway attenuated chronic mechanical pain in a rat model of endometriosis

摘要

The specific role of TLR4 signaling in the pain symptom of endometriosis(EM)remains obscure.The rat endometriosis model was established by transplanting uterine horn tissue into gastrocnemius.W estern blotting and/or immunofluorescent staining were applied to detect high mobility group box 1(HMGB1),TLR4,myeloid differentiation factor-88 adaptor protein(MyD88),and nuclear factor kappa-B-p65(NF-kB-p65)expression,as well as the activation of astrocyte and microglia.The antagonist of TLR4(LPS-RS-Ultra,LRU)and MyD88 homodimerization inhibitory peptide(MIP)were intrathecally administrated to assess the behavioral effects of blocking TLR4 signaling on endometriosis-related pain.We found that HMGB1 was upregulated in the implanted uterine tissue,dorsal root ganglion(DRG),and.