ArticleExperimental and therapeutic medicine2026
Integrated network pharmacology and serum metabolomics to reveal the protective mechanism of methanolic extract of BaiYangJie on cisplatin-induced acute kidney injury in mice.
Article in Experimental and therapeutic medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Cisplatin, a chemotherapeutic drug, produces severe nephrotoxicity and at present, there are no effective drugs to clinically prevent or treat it. In the Dai nationality, BaiYangJie is used to treat poisoning caused by chemicals or drugs. Previous research has demonstrated that the methanolic extract of BaiYangJie (MEAG) can treat cisplatin-induced nephrotoxicity; however, its mechanism of action remains unclear. The aim of the present study was therefore to identify the potential mechanism of action of MEAG in cisplatin nephrotoxicity using a combination of network pharmacology and serum metabolomics. Initially, network pharmacology analysis was used to identify hub targets and signalling pathways involved in the renoprotective effects of MEAG. Subsequently, plasma metabolomics profiling utilising ultra performance liquid chromatography-quadrupole time-of-flight mass spectrometry technology revealed key metabolic alterations and pathway modulations associated with MEAG treatment. Finally, integrated analysis uncovered key molecular mechanisms, which were subsequently validated by western blotting and immunohistochemistry. A total of 13 endogenous metabolites were identified in serum metabolomics, primarily involved in phenylalanine metabolism and in the biosynthesis of phenylalanine, tyrosine and tryptophan. The treatment of MEAG in cis-induced acute kidney injury primarily involved regulating the inflammatory response, responses to lipid and chemical stress, the FoxO signalling pathway, arachidonic acid metabolism and the NF-κB signalling pathway. Animal experiments showed that MEAG can inhibit inflammation and the expression of the migration inhibitory factor (MIF)/NF-κB pathway. Through integrated network pharmacological analysis, metabolomic profiling and experimental validation, it was systematically elucidated that MEAG exerted its therapeutic effects through dual regulatory mechanisms: Suppressing inflammatory responses by inhibiting overactivation of the MIF/NF-κB signalling pathway and restoring phenylalanine metabolic homeostasis. These findings thus provide a mechanistic foundation for developing targeted therapeutic strategies against chemotherapy-associated nephrotoxicity.
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