Allicin ameliorates sepsis-induced acute kidney injury through Nrf2/HO-1 signaling pathway.

ABSTRACT: Acute kidney injury (AKI) is a complication that can be induced by different factors. Allicin is a class of organic sulfur compounds with anticancer and antibacterial effects, and has not been reported in sepsis-induced AKI (S-AKI). S-AKI was induced in c57BL/6 mice by cecal ligation puncture. In response to the treatment of allicin, the survival rate of mice with S-AKI was increased. Reduced levels of serum creatinine, blood urea nitrogen, UALB, KIM-1 and NGAL indicated an improvement in renal function of S-AKI mice. Allicin inhibited the inflammation and cell apoptosis, which evidenced by decreased levels of inflammatory cytokines and apoptosis-related proteins. Oxidative stress was evaluated by the levels of oxidative stress biomarkers, and suppressed by allicin. In addition, allicin-al

SUBMITTER: Li XJ 

PROVIDER: S-EPMC10764392 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature