Traditional Chinese medicine has specific effect on some chronic diseases in clinic, especially in rheumatic diseases. Tripterygium wilfordii Hook (TWH) is a traditional Chinese medicine commonly used in the treatment of rheumatoid arthritis (RA); the unique therapeutic effect has been confirmed by a large number of research papers. TWH has many compounds that lead to its active compounds. However, the potential targets and pharmacological and molecular mechanism of its action treatment of rheumatic diseases are not entirely clear. Therefore, the network pharmacology approach is needed to further study and explore its treatment mechanism. We have successfully set up 10 networks, including four major networks and other networks. Four major networks include rheumatoid arthritis disease network, compound-compound target network of TWH, TWH compound target-rheumatoid arthritis disease network, and TWH-rheumatoid arthritis disease-mechanism network. Other networks consist of RA disease and TWH related targets clusters, biological processes, and pathways network. Our study successfully predicted, explained, and confirmed the TWH of RA disease molecular synergy and found the potential of RA related targets, cluster, biological process, and pathways. This study not only provides prompts to the researcher who explores pharmacological and biological molecular mechanism of TWH applying to RA disease, but also proves a feasible method for discovering potential activated compounds from Chinese herbs.

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Articular cartilage damage and chondrocyte apoptosis are common features of rheumatoid arthritis and osteoarthritis. Recently, curcumin has been reported to exhibit protective effects on degeneration in articular cartilage diseases. However, the effects and mechanisms of curcumin on articular chondrocyte injury remain to be elucidated. The aim of the present study is to investigate the chondroprotective mechanisms of curcumin on interleukin‐1β (IL‐1β)‐induced chondrocyte apoptosis in vitro. The results revealed that IL‐1β decreased cell viability and induced apoptosis in primary articular chondrocytes. Curcumin pretreatment reduced IL‐1β‐induced articular chondrocyte apoptosis. In addition, treatment with curcumin increased autophagy in articular chondrocytes and protected against IL‐1β‐induced apoptosis. The curcumin‐mediated protection against IL‐1β induced apoptosis was abolished when cells were treated with the autophagy inhibitor 3‐methyladenine or transfected with Beclin‐1 small interfering RNA. Furthermore, IL‐1β stimulation significantly increased the phosphorylation levels of nuclear factor (NF)‐κB p65 and glycogen synthase kinase‐3β, and decreased the phosphorylation levels of β‐catenin in articular chondrocytes, and these alterations to the phosphorylation levels were partly reversed by treatment with curcumin. Dual‐luciferase and electrophoretic mobility shift assays demonstrated that IL‐1β increased NF‐κB p65 promoter activity in chondrocytes, and this was also reversed by curcumin. Pretreatment with the NF‐κB inhibitor pyrrolidine dithiocarbamate enhanced the protective effects of curcumin on chondrocyte apoptosis, but Wnt/β‐catenin inhibitor, XAV‐939, did not exhibit this effect. Molecular docking and dynamic simulation studies results showed that curcumin could bound to RelA (p65) protein. These results indicate that curcumin may suppress IL‐1β‐induced chondrocyte apoptosis through activating autophagy and restraining NF‐κB signaling pathway.

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Background: Yiganling (YGL) capsule is a traditional Chinese medicine preparation consisting of eight herbs that has been clinically proven to have a favorable treatment effect on Hepatitis B (HB). However, due to its multiple targets and multi-pharmacological effects, the mechanisms of YGL capsule in the treatment of HB are unknown. Methods: First, the chemical constituents of YGL capsules were obtained from the Chinese medicine database, and YGL capsules were constructed. Second, active compounds were screened by the ADME model. The target fishing model was used to screen the corresponding targets of active compounds and to construct a compounds and compound targets network. Using human disease databases and literature mining, we systematically identified genes associated with HB, constructed disease-specific protein-protein interaction networks, and performed clustering and enrichment analyses of these networks. These networks were then merged to obtain a compounddisease target network, and cluster and enrichment analyses were performed on the compound-disease target network to acquire a compounds-disease targets-mechanism network and a clustering network. Results: We successfully built eight pharmacological network diagrams, including four primary networks and other network maps. The four dominating network maps included a HB disease-associated protein-protein interaction network, a YGL capsule compounds-target network, a YGL capsule ingredient target-HB disease target network, and a YGL-HB disease mechanism network. Other networks included a pathway of HB disease targets, the HB disease protein-protein interaction cluster analysis network, and the YGL-HB target clustering network. Conclusion: This study successfully forecasted, illuminated, and confirmed the synergistic effects of HB disease molecules and discovered the potential of HB relevant targets, clusters, and target-related biological processes and signaling pathways. Our research not only provides theoretical support for the molecular and pharmacological mechanisms of YGL capsule in HB treatment, but also provides new research methods for the study of the other traditional Chinese medicinal compounds.