[Toll-like Receptor 4/Nuclear Factor-κB Signaling in Synovial Tissue Is Involved in the Anti-inflammatory Effect of Moxibustion in Rats with Rheumatoid Arthritis].

医学 炎症 类风湿性关节炎 肿瘤坏死因子α NF-κB 关节炎 内科学 消炎药 促炎细胞因子 滑膜 艾灸 TLR4型 免疫学 脂多糖 药理学 受体
作者
Chuan-ying Zhang,Ling Hu,Rong-Lin Cai,Chuan-Yu Peng,Juan Yuan
出处
期刊:Acupuncture Research 卷期号:43 (11): 687-691 被引量:4
标识
DOI:10.13702/j.1000-0607.180229
摘要

Objective To observe the effect of moxibustion on Toll-like receptor 4/nuclear factor-κB (TLR 4/NF-κB) signaling in the synovial tissue of the ankle joint in rats with rheumatoid arthritis (RA), so as to analyze its biological mechanism underlying improvement of RA. Methods Fifty male SD rats were randomly divided into normal control, model, moxibustion, moxibustion + TLR 4 agonist, and moxibustion + TLR 4 antagonist groups (n=10 rats in each). The RA model was established by subcutaneous injection of Freund's complete adjuvant (FCA, 0.1 mL/rat) at the right hind-paw and by being raised in a wind (air fan blowing), cold (about 10 ℃) and wet (purling) environment for 20 days. After 3 days of modeling, mild moxibustion was applied to bilateral Shenshu (BL 23) and Zusanli (ST 36) for 20 minutes, once daily for successive 10 days. The TLR 4 agonist (lipopolysaccharide) or TLR 4 antagonist (TAK-242) (1 mg/mL) was separately administered via the tail vein 30 min before performing moxibustion every time in the agonist group and the antagonist group. The expression of NF-κB inhibitory factor ɑ (IκBɑ), IκB kinase complex β(IκKβ), myeloid differentiation factor 88 (MyD 88), TLR 4, and NF-κB p 65 proteins in the synovial tissue of the ankle joint was detected by using Western blot. Results Following modeling, the girth of the swollen ankle joint was obviously bigger (P 0.05), suggesting that activation of TLR 4 reduced the anti-inflammatory effect of moxibustion intervention. Conclusion Moxibustion can reduce the ankle joint swelling in RA rats, which may be closely associated with its effect in down-regulating the expression of IκBɑ, IκKβ, TLR 4, MyD 88, and NF-κB p 65 proteins and in inhibiting TLR 4/NF-κB signaling in the synovial tissue of the ankle joint.
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