关键词: 萝卜硫素, HMGB1 / TLR4 / MyD88 信号通路, 子宫内膜异位症, 炎性反应, 疼痛

Abstract: Objective Based on the HMGB1 / TLR4 / MyD88 signaling pathway, to explore the effect of sulforaphane on chronic mechanical pain in rats with endometriosis ( EMs) . Method The EMs model was constructed by autologous endometrial tissue transplantation in rats. The rats were divided into sham operation group ( sham group) , EMs group, sulforaphane low-dose group (5 mg / kg) , sulforaphane high-dose group ( 15 mg / kg) , HMGB1 inhibitor group ( EP group) , and TLR4 inhibitor group ( TAK-242 group) . The pain threshold of rats was detected by an electronic pain meter; the levels of HMGB1, TNFα, IL-6 and IL-10 in rat serum were detected by ELISA; the protein levels of HMGB1, TLR4, MyD88 and TRPV1 in ectopic endometrial tissue were detected by Western blot. Result Compared with the Sham group, the paw withdrawal threshold ( PWT) of the EMs group was lower (P<0. 05) ; the levels of serum HMGB1, TNF-α, IL-6 and IL-10 were higher ( P < 0. 05) ; the expression of HMGB1, TLR4, MyD88 and TRPV1 proteins in ectopic endometrial tissue was increased (P<0. 05) . Compared with the EMs group, low and high doses of sulforaphane, HMGB1 inhibitor, and TLR4 inhibitor could increase PWT of rat and reduce levels of serum HMGB1, TNF-α, IL-6 and IL-10, and reduce expression of HMGB1, TLR4, MyD88 and TRPV1 proteins in ectopic endometrial tissue ( P < 0. 05) . Conclusion Sulforaphane can reduce the mechanical pain caused by EMs by inhibiting the HMGB1 / TLR4 / MyD88 signaling pathway.

Key words: sulforaphane, HMGB1 / TLR4 / MyD88 signaling pathway, endometriosis, inflammatory response, pain