Aim:
Background: Sepsis-associated acute kidney injury is prevalent in critically ill patients. A plethora of mechanisms are involved in the etiology of Sepsis-associated acute kidney injury, including metabolic reprogramming and inflammatory responses, diverse forms of cell death, processes of autophagy and efferocytosis, as well as hemodynamic alterations. The phenomenon of SA-AKI was experimentally elicited in murine models via the procedure of cecal ligation and puncture. Aims: to reveal possible protective impact of Eprosartan on sepsis-induced acute kidney injury within the sepsis model.

Material and methods:
Materials and methods: Albino male Swiss mice n=40 were allocated into four distinct groups: (i) Normal group, (ii) CLP 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-κB protein level was notably lessened in the group of CLP+ Eprosartan than that of CLP (p<0.05). Eprosartan treatment attenuated considerable tubular injuries of the sepsis murine group p<0.05.

Conclusions:
Conclusion: our findings unveil that Eprosartan could serve as a promising therapeutic agent in the context of sepsis-induced AKI.