Acute kidney injury (AKI) is a common and serious health issue with a growing incidence and mortality rate. Tripterygium wilfordii (TW) is a traditional Chinese medicine that has been reported to cause kidney damage. However, the associated mechanism of TW-induced AKI remains unclear. Therefore, we aimed to uncover the associated mechanisms of AKI induced by TW using network pharmacology and bioinformatics. The candidate compounds of TW and the potential targets were screened using TCMSP and CTD database, and the AKI-related targets were identified from the DisGeNET database. The disease targets were intersected with the drug targets, and the Wayne diagram was drawn by Venny2.1.0 software. We developed protein-protein interactions (PPI) network and the "disease-compound-target-pathway" network through the Cytoscape software. By using the DAVID database, GO and KEGG enrichment analysis was carried out to reveal the potential signaling pathways of the compound-TW-induced AKI. Meanwhile, the Auto dock vina 1.1.2 was used for molecular docking to verify the active compound and key targets’ binding ability. Critical compounds and key targets of TW-induced AKI were identified, including triptolide, kaempferol, β-sitosterol, nobiletin, stigmasterol, TNF, and so on. The GO analysis showed that potential genes’ biological function was mainly involved in apoptosis, oxidative stress, and inflammation. Moreover, eight signaling pathways were found, including the HIF-1 signaling pathway, VEGF signaling pathway, apoptosis, and so on. The molecular docking results proved that the core compound’s affinity with the corresponding protein of the gene targets was good. This study preliminarily predicted the core toxic compounds, targets, and related pathways of TW-induced AKI, providing a theoretical basis for the follow-up clinical rational drug use and related research work of TW.
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