Abstract

Abstract Ginsenoside Rg1 (G-Rg1) can effectively ameliorate lipopolysaccharide-induced renal injury. The impact and mechanism of G-Rg1 in renal ischemia-reperfusion (I/R) injury are not yet understood. This study aimed to examine the role and mechanism of G-Rg1 in kidney I/R injury. The renal I/R injury mice and mouse kidney cells were applied as renal I/R injury models. Researchers analyzed the functions and mechanisms of G-Rg1 using techniques like cell proliferation, apoptosis, clone formation assay, ELISA, HE staining, immunohistochemical staining, Immunofluorescence staining, qRT-PCR, and Western blot analysis. Our findings indicate that G-Rg1 pretreatment protects against renal I/R injury by lowering serum creatinine and urea nitrogen levels, mitigating histological damage and apoptosis, and reducing inflammation and oxidative stress. These beneficial effects were accompanied by the suppression of fatty acid binding protein 1 (FABP1) and heme oxygenase-1 (HO-1) expression and the promotion of nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation. However, the therapeutic effect of G-Rg1 was inhibited by FABP1 overexpression. The mechanism by which G-Rg1 ameliorates renal I/R injury may be related to the inhibition of FABP1 expression and thus regulation of the Nrf2/HO-1 pathway.