Antipruritic effects of electroacupuncture on morphine-induced pruritus model mice through the TLR2/4-MyD88-NF-κB pathway

电针对吗啡诱发瘙痒模型小鼠通过TLR2/4-MyD88-NF-κB通路的止痒作用

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作者:Yu Shan Ye, Ai Zhen Pan, Yan Zhen, Meng Ru Kang, Bin Zhang, Wei Min Yi

Abstract

Pruritus is one of the common side effects of intrathecal or epidural injection of opioids. The aim of this study was to test the antipruritic effect of acupuncture and its possible mechanism. We used electroacupuncture (EA), toll-like receptor (TLR)2/4 antagonist sparstolonin B (SsnB), and TLR2/4 agonist peptidoglycan (PGN) to precondition female wild-type BALB/c mice, and then prepared a morphine-induced pruritus model. The mRNA and protein expression levels of TLR2, TLR4, MyD88, and NF-κB were detected by RT-PCR and western blotting. The contents of interleukin (IL)-1, IL-6, IL-12, IL-10, and tumor necrosis factor-α in serum were measured by ELISA assays. Flow cytometry was performed to analyze the ratio of M1-phenotype to M2-phenotype macrophages. Our results showed that EA preconditioning improved pruritus; reduced the expressions of TLR2, TLR4, MyD88, and NF-κB both at the mRNA and protein levels (P<0.05); reduced the expression of proinflammatory cytokines IL-1, IL-6, IL-12, and tumor necrosis factor-α; and increased the expression of anti-inflammatory cytokine IL-10 (P<0.05). EA promoted M2-phenotype macrophage differentiation. Moreover, these results showed no significant difference between the SsnB group and the EA+SsnB group (P>0.05), but showed a significant difference between the PGN group and the EA+PGN group (P<0.05). Therefore, we propose that EA may be involved in the remission of pruritus in morphine-induced pruritus model mice through the TLR2/4-MyD88-NF-κB pathway. EA is a potential therapeutic treatment for pruritus.

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