Background: Cisplatin, a chemotherapeutic agent often causes nephrotoxic side effects. Lipopolysaccharide (LPS) is known to induce pro-inflammatory responses, often leading to septic renal injury. We hypothesized that the combination of cisplatin and LPS would amplify renal injury, thereby improving a renal injury model. Therefore, we administered both agents to mice and evaluated renal injury indicators. Methods: Eight-week-old male C57BL/6 mice were injected with cisplatin (8, 10, or 12 mg/kg) and LPS (5 mg/kg) on days 1 and 4 following of each week. Mice were euthanized at specific time points to assess renal injury. Body weight, renal weight, area, and BUN levels were measured to evaluate renal damage. Additionally, hematoxylin and eosin (H&E) and Masson’s trichrome (MT) staining were performed to assess histological changes. Results: The combination of cisplatin and LPS significantly reduced body and renal weight compared to cisplatin alone. A high dose of cisplatin (12 mg/kg) resulted in a 50% mortality, while, lower doses (8 and 10 mg/kg) showed 100% survival. Significant renal injury was observed in the 10 mg/kg cisplatin group administered for two weeks. In the 8 mg/kg cisplatin group, no changes were observed after two weeks, but renal damage appeared after four weeks. Histological evaluations in the 10 mg/kg cisplatin group administered for two weeks showed renal injury features, including tubular damage and fibrosis. Conclusions: Administering cisplatin (10 mg/kg) with LPS for two weeks or cisplatin (8 mg/kg) with LPS for four weeks resulted in a distinct renal injury, effectively establishing a renal injury mouse model.

ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
    Chemical induced-renal injury model
    Immunohistochemistry
    Assessments of BUN
    Statistical analysis
RESULTS
    Effect of cisplatin and LPS co-administration togenerate renal injury model
    Dose and duration-dependent effects of cisplatin andLPS co-administration
    Histological abnormality and fibrosis in renal injurymouse model
DISCUSSION
CONCLUSION
REFERENCES

• Sae-Byeok Hwang(Cell Therapy 3 Center, CHA Advanced Research Institute, CHA Bundang Medical Center, Seongnam 13488, Korea, Department of Biomaterials Engineering, School of Medicine and Biomedical Science, College of Life Science, CHA University, Seongnam 13488, Korea)
• Soon-Suk Kang(Cell Therapy 3 Center, CHA Advanced Research Institute, CHA Bundang Medical Center, Seongnam 13488, Korea)
• Yeonmi Lee(Cell Therapy 3 Center, CHA Advanced Research Institute, CHA Bundang Medical Center, Seongnam 13488, Korea, Department of Biochemistry, School of Medicine and Biomedical Science, College of Life Science, CHA University, Seongnam 13488, Korea)
• Eunju Kang(Cell Therapy 3 Center, CHA Advanced Research Institute, CHA Bundang Medical Center, Seongnam 13488, Korea, Department of Biochemistry, School of Medicine and Biomedical Science, College of Life Science, CHA University, Seongnam 13488, Korea) Corresponding author