首页|Moxibustion inhibits the macrophage M1 polarization toll-like receptor 4/myeloid differentiation factor 88/nuclear factor kappa B signaling pathway by regulating T-cell immunoglobulin and mucin-containing protein-3 in rheumatoid arthritis
Moxibustion inhibits the macrophage M1 polarization toll-like receptor 4/myeloid differentiation factor 88/nuclear factor kappa B signaling pathway by regulating T-cell immunoglobulin and mucin-containing protein-3 in rheumatoid arthritis
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维普
OBJECTIVE:To explore whether moxibustion exerts therapeutic effects on rheumatoid arthritis(RA)by regulating the expression of T-cell immunoglobulin and mucin-containing protein-3(TIM-3)and subsequently modulating the macrophage M1 polarization toll-like receptor 4(TLR4)-myeloid differentiation factor 88(MyD88)-nuclear factor kappa B(NF-κB)signaling pathway.METHODS:We utilized moxibustion treatment in RA rat models using the Zusanli(ST36)and Shenshu(BL23)acupoints.Hematoxylin and eosin(HE)staining was used to observe the pathological changes of the synovial tissue under a section light microscope,and pathological scoring was performed according to the grading standard of the degree of synovial tissue disease.Enzyme-linked immunosorbent assay(ELISA)was applied to verify the efficacy of moxibustion in reducing inflammation.Quantitative real-time polymerase chain reaction(qRT-PCR)was used to detect the expression of the TIM-3/TLR4-MyD88-NF-κB signaling pathway-related molecules,and Western blot was used to detect the contents of synovial NF-κB.RESULTS:We established the Freund's complete adjuvant(FCA)-induced RA model in rats.The expression level of M1 polarization signaling pathway TLR4-MyD88-NF-κB and the inflammatory factors interleukin-12(IL-12),tumor necrosis factor alpha(TNF-α),and tumor necrosis factor beta(TNF-β)were significantly increased in the RA model.After moxibustion treatment,the expression level of TLR4-MyD88-NF-κB was significantly decreased,and the inflammatory factors IL-12,TNF-α,and TNF-β were decreased,but the expression level was significantly increased in the RA model.When TIM-3 expression was inhibited,the expression level of TLR4-MyD88-NF-κB,and the inflammatory factors IL-12,TNF-α,and TNF-β were not suppressed,even after moxibustion treatment.CONCLUSIONS:Moxibustion regulates the key target TIM-3 by acting on the Zusanli(ST36)and Shenshu(BL23)points,thereby inhibiting the M1 polarization of macrophages;that is,it inhibits the TLR4-MyD88-NF-κB signaling pathway,and finally achieves alleviation of pathological changes and anti-inflammatory effects.
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