Objective:To observe the regulatory effects of Tongfenglian capsule on intestinal flora,inflammatory factors and other indicators of gout in rats with gout arthritis(GA),and to explore possible mechanism of Tongfengli capsule on GA.Methods:A total of 36 male SD rats were randomly divided into blank group,Tongfenglian low,medium and high doses(0.216 g/kg,0.432 g/kg,0.864 g/kg)groups,colchicine group(0.18 mg/kg)and model group.Blank group and model group were given the same amount of distilled water,other groups were given the corresponding drug once a day for 14 days.On the 13th day after gavage,GA rat models were prepared according to Coderre modeling method,0.2 ml normal saline was injected into the right ankle joint for blank group,and general conditions of rats were dynamically observed to determine whether the model was established,and the time was recorded.Rate of foot swelling in each group was calculated.Abdominal aorta blood,colon tissue and intestinal contents of rats were collected,and colon length,pathological changes of colon tissue,serum levels of inflammatory factors(IL-1β,TLR4),mRNA expressions of NF-κB and TLR4 inflammatory pathway in intestinal tissue,and intestinal flora of rats were detected.Results:Compared with blank group,swelling rate of ankle joint,serum IL-1β and TLR4 levels,and mRNA expressions of TLR4 and NF-κB in intestinal tis-sue were significantly increased in model group,and a large number of inflammatory cells were infiltrated in the colon by HE staining,showing typical inflammatory pathological changes,colon length decreased significantly,intestinal flora richness and diversity de-creased,ratio of Firmicutes to Bacteroidetes increased,the abundance of Lactobacillus and Bifidobacterium decreased,and the abun-dance of Prevotella and Escherichia coli-Shigella increased.Compared with model group,all the indexes in all Tongfenglian groups were improved,the richness and diversity of intestinal flora were increased,and the reduction of intestinal microbial diversity and mi-crobial community structure caused by monosodiumurate were changed.Conclusion:Mechanism of Tongfenglian capsule alleviating inflammation may be related to the regulation of TLRs/NF-κB signaling pathway.Through the mediation of intestinal flora,Tongfengli-an capsule plays a role in regulating intestinal homeostasis,improving the abundance and diversity of intestinal microorganisms,and playing an intervention role in GA.This microecological intervention mechanism may be a potential means to prevent and treat GA.

Objective:To observe the regulatory effects of Tongfenglian capsule on intestinal flora,inflammatory factors and other indicators of gout in rats with gout arthritis(GA),and to explore possible mechanism of Tongfengli capsule on GA.Methods:A total of 36 male SD rats were randomly divided into blank group,Tongfenglian low,medium and high doses(0.216 g/kg,0.432 g/kg,0.864 g/kg)groups,colchicine group(0.18 mg/kg)and model group.Blank group and model group were given the same amount of distilled water,other groups were given the corresponding drug once a day for 14 days.On the 13th day after gavage,GA rat models were prepared according to Coderre modeling method,0.2 ml normal saline was injected into the right ankle joint for blank group,and general conditions of rats were dynamically observed to determine whether the model was established,and the time was recorded.Rate of foot swelling in each group was calculated.Abdominal aorta blood,colon tissue and intestinal contents of rats were collected,and colon length,pathological changes of colon tissue,serum levels of inflammatory factors(IL-1β,TLR4),mRNA expressions of NF-κB and TLR4 inflammatory pathway in intestinal tissue,and intestinal flora of rats were detected.Results:Compared with blank group,swelling rate of ankle joint,serum IL-1β and TLR4 levels,and mRNA expressions of TLR4 and NF-κB in intestinal tis-sue were significantly increased in model group,and a large number of inflammatory cells were infiltrated in the colon by HE staining,showing typical inflammatory pathological changes,colon length decreased significantly,intestinal flora richness and diversity de-creased,ratio of Firmicutes to Bacteroidetes increased,the abundance of Lactobacillus and Bifidobacterium decreased,and the abun-dance of Prevotella and Escherichia coli-Shigella increased.Compared with model group,all the indexes in all Tongfenglian groups were improved,the richness and diversity of intestinal flora were increased,and the reduction of intestinal microbial diversity and mi-crobial community structure caused by monosodiumurate were changed.Conclusion:Mechanism of Tongfenglian capsule alleviating inflammation may be related to the regulation of TLRs/NF-κB signaling pathway.Through the mediation of intestinal flora,Tongfengli-an capsule plays a role in regulating intestinal homeostasis,improving the abundance and diversity of intestinal microorganisms,and playing an intervention role in GA.This microecological intervention mechanism may be a potential means to prevent and treat GA.

Objective:To explore the gene microarray of patients with ankylosing spondylitis in GEO database by using various bioinformatics methods, and to explore the possible targets and mechanisms of action.Methods:The GEO database was searched with "ankylosing spondylitis" the keyword, and the expression profile of genes related to AS was selected as the research object. Standard difference analysis, weighted co-expression analysis and gene set enrichment analysis were conducted to construct the disease set. GO and KEGG enrichment analysis were performed on the disease sets. The NCC algorithm identifies the first five key genes. THP-1 cells were implanted into RPMI-1640 culture medium containing 10% fetal bovine serum to multiply and construct the cell model of AS in vitro. The expression levels of 5 key genes were detected by qRT-PCR and Western blot. The experimental measurement data were expressed as mean± standard deviation, and the t test was used in comparison between the two groups. Results:One thousand six hundred and sixty seven disease genes were analyzed, functional annotation was mainly concentrated in 689 molecular components of cytoplasmic ribosomes, ribosomal subunits, ribosomes, cytoplasmic large ribosomal subunits, the structural composition of ribosomal REDOX enzyme activity, 1 002 molecular functions of NADH dehydrogenase activity, NADH dehydrogenase activity, and 5 764 molecular processes of mRNA catabolism and RNA catabolism The physical process involved 1 002 signaling pathways involved in Alzheimer′s disease, Prion disease, Parkinson′s disease, and the first 5 key genes were identified as RPS11, RPL4, RPL37A, RPS23, and RPS9. The experimental results were obtained by t test. The results showed that TNF-α mRNA ( t=5.59, P=0.001) and protein ( t=20.14, P<0.001) were significantly increased, indicating that LPS had induced inflammatory response in THP-1 cells, while RPL37AmRNA ( t=5.87, P=0.001), RPS11 mRNA ( t=3.88, P=0.008), RPS23 mRNA ( t=2.64, P=0.038), RPL37A protein ( t=3.18, P=0.030), RPS11 protein ( t=11.26, P<0.001), RPS23 protein ( t=5.64, P<0.001), increased, while RPS9 mRNA ( t=3.16, P=0.020), RPL4 mRNA ( t=2.54, P=0.044), RPS9 protein ( t=5.85, P<0.001) and RPL4 ( t=2.93, P=0.040) protein expressions decreased. RPL23 stimulated the joint synovial tissue to produce effect-T lymphocytes and release a large number of IL-2 and other inflammatory cytokines. RPS9 acts on the early stages of ribosomogenesis, and knocking down RPS9 reduced overall protein synthesis. RPL4 interacted with TTC22 protein to enhance the binding of WTAP mRNA to RPL4, which was associated with immune diseases. The nucleoprotein OGFOD1 catalyzed the hydroxylation of RPS23 and participated in the inflammatory process. The chromosome conformation confirmed the single nucleotide polymorphism function of IL23R genomic locus in AS disease. Conclusion:Ribosomal protein may be an important target for exploring the mechanism of AS inflammation.