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Background. Scutellaria baicalensis Georgi (SBG) has significant anti-inflammatory and immune-modulating activities and is widely used in the treatment of inflammatory and autoimmune diseases. However, the mechanism of SBG in the treatment of ankylosing spondylitis (AS) remains to be elucidated. Methods. Differentially expressed genes (DEGs) related to AS were analyzed based on two GEO gene chips. The DEGs were merged with the data derived from OMIM, GeneCards, and PharmGKB databases to ascertain AS-related targets. Active components of SBG and their targets were acquired from the TCMSP database. After overlapping the targets of AS and SBG, the action targets were acquired. Subsequently, protein-protein interaction (PPI) network and core target screening were conducted using the STRING database and Cytoscape software. Moreover, the DAVID platform was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of action targets. Finally, the affinity of major active components and core targets was validated with molecular docking. Results. A total of 36 active components of SBG were acquired from TCMSP database. Among these, the main active components were baicalein, wogonin, and oroxylin A. The PPI network and screening showed TNF, IL-6, CXCL8, PTGS2, and VEGFA as core targets associated SBG against AS. GO and KEGG analyses indicated that SBG participated in various biological processes, via regulating IL-17, TNF, and NF-κB signaling pathways. Molecular docking results confirmed a strong binding activity between the main active components and the core targets. Conclusion. The therapeutic mechanism of SBG associated with AS can be characterized as a multicomponent, multitarget, and multipathway mechanism. SBG may be a promising therapeutic candidate for AS. [ABSTRACT FROM AUTHOR]

Radix Salvia miltiorrhiza (RSM) is widely used for the clinical improvement of inflammatory diseases. However, the actions of RSM in the treatment of ankylosing spondylitis (AS) have not been fully explored. Therefore, this study was designed to use retrospective clinical data mining approach to understand the effects of RSM on AS-related immuno-inflammatory processes, use network pharmacology to predict therapeutic targets of RSM, and to further investigate the pharmacological molecular mechanism in vitro. RSM treatment has a long-term correlation with the improvement of AS-related immuno-inflammatory indicators through computational models. We established protein-protein interaction networks, conducted KEGG analysis to enrich significant TNF pathways, and finally obtained three core targets of RSM in the treatment of AS, namely, prostaglandin endoperoxide synthase 2 (PTGS2), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). Screening of RSM active ingredients with node degree greater than 20 yielded cryptotanshinone and tanshinone IIA, and previous studies have reported their anti-inflammatory effects. In vitro, both cryptotanshinone and tanshinone IIA significantly inhibited the expressions of PTGS2, IL-6, and TNF-α in peripheral blood mononuclear cells in AS patients. In conclusion, cryptotanshinone and tanshinone IIA, which are the active components of RSM, may inhibit the activation of TNF signaling pathway in AS patients by downregulating the expression of PTGS2, IL-6, and TNF-α. These findings illustrate that RSM may be a promising therapeutic candidate for AS, but further validation is required. [ABSTRACT FROM AUTHOR]