In the present study effect of piperazine-benzamide was investigated on pathological damage associated with AKI in mice model in vivo. The mice model of AKI was established by cecal ligation and puncture surgery procedure and levels of TNF-alpha as well as IL-1 beta were determined by ELISA assay. Western blotting was used to measure protein expression and hematoxylin and eosin (H&E) for detection of pathological damage. A significant increase in survival rate of AKI mice was observed in mice by piperazine-benzamide treatment. Piperazine-benzamide treatment of the mice reversed AKI-induced increase in creatinine and blood urea nitrogen level. Renal injury development by AKI in mice was also prevented significantly on treatment with piperazine-benzamide. Treatment with piperazine-benzamide reversed AKI-induced production of IL-1 beta, IL-18 and TNF-alpha in mice renal tissues. The AKI-mediated promotion of Bax expression was inhibited while as Bcl-2 level was promoted in mice renal tissues by piperazine-benzamide treatment. Thus, piperazine-benzamide treatment improves survival rate and prevents kidney damage induced by sepsis in mice. It inhibits production of inflammatory cytokines and raises expression of Bcl-2 protein in AKI mice. Therefore, piperazine-benzamide may be used for the treatment of kidney damage associated with sepsis.