Effect of electroacupuncture on alleviating experimental rheumatoid arthritis in rats by restoring gut microbiota and inhibiting LPS-TLR4-NF-κB axis
Objective To explore the effect of electroacupuncture on alleviating experimental rheumatoid arthritis (RA) in rats by restoring intestinal microbiota and inhibiting LPS-TLR4-NF-κB axis. Methods 10 rats were randomly selected as the normal group from 50 clean Wistar male rats,and the remaining 40 rats were used to establish RA rat models. The model mice were randomly divided into the model group and the electroacupuncture group,in which the electroacupuncture group was treated with electroacupuncture therapy,while the normal group and the model group were not treated. The joint swelling degree (JSD) and arthritis index (AI) in the model group and electroacupuncture group at different time points were recorded. After the experiment,the changes of joint ultrastructure and intestinal microflora,levels of inflammatory factors,and expression of LPS-TLR4-NF-κB signaling pathway factors mRNA and protein in each group were observed. Results After intervention,JSD and AI in the electroacupuncture group were significantly lower than those in the model group (P＜0.05). Compared with the normal group,the model group had synovial tissue proliferation,severe and incomplete cell membrane destruction,and a large number of inflammatory cell infiltration;After electroacupuncture treatment,the synovial tissue proliferation,inflammatory cell infiltration,rough endoplasmic reticulum expansion in rats were significantly improved,and the nuclear membrane margin was clear. Compared with the model group,the relative abundance of intestinal microbiota,levels of inflammatory factors,and LPS-TLR4-NF-κB signaling pathway related mRNA levels in the electroacupuncture group were improved (P＜0.05). Conclusion Electroacupuncture therapy can effectively improve joint symptoms and inhibit the expression of inflammatory factors in RA rats,and its mechanism may be related to the regulation of intestinal microbiota and the inhibition of LPS-TLR4-NF-κB signaling pathway.
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