Renal protective effects of Eprosartan in sepsis: Targeting NF-κB and apoptotic pathways.

Abstract

OBJECTIVE: Aim: To reveal possible protective impact of Eprosartan on sepsis-induced acute kidney injury within the sepsis model. PATIENTS AND METHODS: Materials and Methods: Albino male Swiss mice (n=40) were allocated into four distinct groups: (I) Normal group, (II) Cecal ligation & puncture group, (III) Vehicle group, and (IV) CLP + Eprosartan group (60 mg/kg one hour before CLP intraperitoneally). Blood and tissue biochemical/routine indicators, renal function, SA-AKI-related pathophysiological processes, and nuclear factor kappa B p65 gene expression in septic mice were assessed by histological hematoxylin and eosin staining, quantitative real-time polymerase chain reaction, and Enzyme-Linked Immunosorbent Assay. RESULTS: Results: Our findings highlight that Eprosartan reversed CLP-provoked increased serum blood urea nitrogen, creatinine (as well as kidney injury molecule levels. It also significantly inhibited the elevated concentrations of tumor necrosis factor alpha and caspase-3 within the tissue. Additionally, NF-&#x3ba;B gene expression level was notably lessened in the group of CLP+ Eprosartan than that of CLP (p<0.05). Eprosartan treatment attenuated considerable tubular injuries in the sepsis murine group p<0.05. CONCLUSION: Conclusions: our findings unveil that Eprosartan could serve as a promising therapeutic agent in the context of sepsis-induced AKI.