The Kininogen 1/bradykinin receptor B2 system serves as a key molecular response of vancomycin-induced nephrotoxicity and may be a potential target of absinthin.

OBJECTIVE: The occurrence of nephrotoxicity induced by Vancomycin (Van) has been documented in both experimental models and clinical patients. In this study, we aimed to identify potential gene targets by utilizing Gene Expression Omnibus (GEO) datasets and a Van-induced mouse model. METHODS: Differentially expressed genes (DEGs) were filtered using GEO datasets (GSE7793), and a mouse model of nephrotoxicity was established by administering Van (400 mg/kg/day for 7 days) via intravenous injection. RESULTS: were significantly increased in Van-treated mice compared with normal mice. Furthermore, we found that absinthin acts as a potential inhibitor of Bdkrb2 and effectively ameliorates Van-induced podocyte apoptosis and reduces the levels of renal injury biomarkers, including serum creatinine (Cre), blood urea nitrogen (BUN), and malondialdehyde (MDA). CONCLUSIONS: Our findings suggest that targeting Kng1/Bdkrb2 may offer a potential therapeutic strategy for mitigating Van-induced nephrotoxicity. These findings suggest that absinthin may serve as a renal protective agent against drug-induced nephrotoxicity.