ObjectiveTo predict the targets and signaling pathways of Si Junzitang and Tongxie Yaofang in treating ulcerative colitis （UC） following the concept of "same disease with different treatments" based on the network pharmacology and explore the underlying mechanisms. MethodThe differentially expressed genes （DEGs） of UC were extracted from GeoChip. The active components and corresponding potential targets of Si Junzitang and Tongxie Yaofang were collected from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform（TCMSP）. The regulatory networks of Si Junzitang and Tongxie Yaofang were constructed and the protein-protein interaction （PPI） network was plotted. The core genes were predicted， followed by enrichment analysis. The UC model was induced in mice by dextran sodium sulfate （DSS） solution. Mice were randomly divided into a normal group， a UC group， a Si Junzitang group， a Tongxie Yaofang group， and a mesalazine group. Drugs were administered continuously for 14 days. The disease activity index （DAI） was scored for mice in each group. The characteristic values of hemorheology were measured. The serum levels of interleukin-6 （IL-6）， tissue factor （TF）， and hypoxia-inducible factor-1α （HIF-1α） in mice were detected. The relative mRNA expression levels of inhibitory kappa B kinase α （IKKα）， nuclear factor kappa B （NF-κB）， HIF-1α， and vascular endothelial growth factor （VEGF） were measured. ResultA total of 44 genes were obtained by network pharmacological analysis， including 17 common genes. HIF-1 pathway and hypoxia response were potential common targets of Si Junzitang and Tongxie Yaofang in the treatment of UC. The results showed that Si Junzitang and Tongxie Yaofang could significantly reduce DAI score， increase blood perfusion volume and blood cell movement speed， decrease the concentration of mobile red blood cells， reduce the levels of IL-6， TF， and HIF-1α， down-regulate the mRNA expression of IKKα， NF-κB， HIF-1α， and VEGF. ConclusionThe HIF-1 pathway and related targets may be the common targets of Si Junzitang and Tongxie Yaofang to exert different therapeutic effects on the same disease. Si Junzitang is potent in promoting Qi circulation to improve intestinal tissue hypoxia， and Tongxie Yaofang is effective in promoting blood circulation to facilitate intestinal mucosal microcirculation.

Objective To explore the targets and pathways of Cynanchum wilfordii for treatment of ulcerative colitis(UC).Methods UPLC-QE-MS was used to identify the components of Cynanchum wilfordii ethanol extract,and their targets were screened using public databases for construction of the core protein-protein interaction(PPI)network and GO and KEGG enrichment analyses.Forty male C57 mice were randomized into normal control group,model group,mesalazine group and Cynanchum wilfordii group(n=10),and in the latter 3 groups,mouse UC models were established by treatment with 2.5%DSS and the latter 2 groups drug interventions by gavage.The therapeutic effect was evaluated by recording body weight changes and DAI score.Pathological changes of the colon tissue were observed with HE and AB-PAS staining,and JAK2 and STAT3 protein expressions were detected with Western blotting.The metabolites and metabolic pathways were identified by metabonomics analysis.Results We identified 240 chemical components in Cynanchum wilfordii alcoholic extracts,including 19 steroids.A total of 177 Cynanchum wilfordii targets,5406 UC genes,and 117 intersection genes were obtained.JAK2 and STAT3 were the core targets and significantly enriched in lipid and atherosclerosis pathways.Cynanchum wilfordii treatment significantly increased the body weight and decreased DAI score of UC mice(P<0.05),alleviated intestinal pathologies,and decreased JAK2 and STAT3 protein expressions in the colon tissues.Most of the 83 intersecting differential metabolites between the control,model and Cynanchum wilfordii groups were identified as glycerophospholipids,arachidonic acid,and amino acids involving glycerophospholipid metabolism and other pathways.Correlation analysis suggested that the core targets of Cynanchum wilfordii for UC participated in regulation of the metabolites.Conclusion Cynanchum wilfordii alleviates lipid and amino acid metabolism disorders to lessen UC in mice by regulating the core targets including JAK2 and STAT3 and the levels of endogenous metabolites.

Objective To explore the targets and pathways of Cynanchum wilfordii for treatment of ulcerative colitis(UC).Methods UPLC-QE-MS was used to identify the components of Cynanchum wilfordii ethanol extract,and their targets were screened using public databases for construction of the core protein-protein interaction(PPI)network and GO and KEGG enrichment analyses.Forty male C57 mice were randomized into normal control group,model group,mesalazine group and Cynanchum wilfordii group(n=10),and in the latter 3 groups,mouse UC models were established by treatment with 2.5%DSS and the latter 2 groups drug interventions by gavage.The therapeutic effect was evaluated by recording body weight changes and DAI score.Pathological changes of the colon tissue were observed with HE and AB-PAS staining,and JAK2 and STAT3 protein expressions were detected with Western blotting.The metabolites and metabolic pathways were identified by metabonomics analysis.Results We identified 240 chemical components in Cynanchum wilfordii alcoholic extracts,including 19 steroids.A total of 177 Cynanchum wilfordii targets,5406 UC genes,and 117 intersection genes were obtained.JAK2 and STAT3 were the core targets and significantly enriched in lipid and atherosclerosis pathways.Cynanchum wilfordii treatment significantly increased the body weight and decreased DAI score of UC mice(P<0.05),alleviated intestinal pathologies,and decreased JAK2 and STAT3 protein expressions in the colon tissues.Most of the 83 intersecting differential metabolites between the control,model and Cynanchum wilfordii groups were identified as glycerophospholipids,arachidonic acid,and amino acids involving glycerophospholipid metabolism and other pathways.Correlation analysis suggested that the core targets of Cynanchum wilfordii for UC participated in regulation of the metabolites.Conclusion Cynanchum wilfordii alleviates lipid and amino acid metabolism disorders to lessen UC in mice by regulating the core targets including JAK2 and STAT3 and the levels of endogenous metabolites.