Society of Diabetic Nephropathy Prevention Journal of Nephropharmacology 2345-4202 15 2 2026 07 01 Therapeutic potential of rosuvastatin in sepsis-induced acute kidney injury; evidence from an experimental animal study e12798 e12798 10.34172/npj.2025.12798 EN Ghanim M. Al-ghanimi https://orcid.org/0009-0009-3226-1145 Ali M. Janabi https://orcid.org/0000-0002-8569-7964 Journal Article 10.34172/npj.2025.12798 2025 05 24 2025 07 09 Introduction: Sepsis-induced acute kidney injury (SI-AKI) is a critical complication contributing to high morbidity and mortality in septic patients. Rosuvastatin, a β-hydroxy β-methylglutaryl-CoA reductase inhibitor widely administered for hyperlipidemia, has demonstrated anti-inflammatory and organ-protective effects in various experimental models. Objectives: This study aims to evaluate the therapeutic potential of rosuvastatin in ameliorating sepsis-induced AKI using an established experimental animal model. Materials and Methods: This experimental animal study was conducted at the university of Kufa, Iraq. Twenty-four adult Swiss albino mice were divided into four groups randomly (n = 6 in each group): Sham group, cecal ligation and puncture (CLP), CLP + dimethyl sulfoxide (DMSO), and CLP + rosuvastatin. The sham group of mice had no CLP laparotomy operation. The CLP group had a midline laparotomy with cecum ligation and perforation. In the CLP + rosuvastatin and CLP + DMSO groups, respectively, a dose of rosuvastatin 10 mg/kg and DMSO was administered intraperitoneally one hour before the CLP process. Kidney function parameters, including serum urea, creatinine, kidney injury molecule-1 (KIM-1) levels, histopathological scores, and nuclear phosphorylated extracellular signal-regulated kinases 1 and 2 (p-ERK 1/2) expression, were measured and compared between four groups. Results: The results demonstrated that sepsis induced by CLP significantly elevated all kidney function parameters, including serum urea, creatinine, KIM-1 levels, histopathological scores, and nuclear p-ERK1/2 expression. However, treatment with rosuvastatin markedly reduced these markers, restoring them to levels comparable to those observed in healthy control mice (sham group), indicating a protective effect of rosuvastatin against sepsis-associated kidney injury. Conclusion: Our study showed that, CLP-induced sepsis caused significant kidney injury, as shown by increased serum markers, tissue damage, and p-ERK1/2 expressions. We also found, treatment with rosuvastatin effectively reduced these changes, restoring kidney function and structure to near-normal levels. These results highlight rosuvastatin’s potential as a protective agent against sepsis-related AKI, likely through modulation of the ERK1/2 pathway.