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Cytokine array after cyclosporine treatment in rats
1Dongsan Kidney Institute and Chronic Disease Research Center, Keimyung University, Daegu, Korea.
Transplantation Proceedings
|October 22, 2008
Summary
Long-term cyclosporine (CsA) treatment causes kidney damage. This study found elevated levels of lipopolysaccharide-induced CXC chemokine (LIX), monocyte chemoattractant protein 1 (MCP-1), nerve growth factor (beta-NGF), and tissue inhibitor of metalloproteinase-1 (TIMP-1) in rats with CsA-induced nephrotoxicity.
Area of Science:
- Nephrology
- Immunology
- Biochemistry
Background:
- Long-term cyclosporine (CsA) administration is associated with chronic nephrotoxicity.
- Cytokines play critical roles in immune responses and various disease processes, including kidney damage.
Purpose of the Study:
- To investigate changes in cytokine profiles in a rat model of CsA-induced chronic nephrotoxicity.
- To identify specific cytokines contributing to CsA-induced kidney damage.
Main Methods:
- A rat model was established with two groups: normal controls and CsA-treated.
- Serum samples were analyzed using a cytokine antibody array to assess protein expression levels.
Main Results:
- CsA-treated rats showed increased serum creatinine, urine creatinine, and creatinine clearance.
- Elevated levels of lipopolysaccharide-induced CXC chemokine (LIX), monocyte chemoattractant protein 1 (MCP-1), nerve growth factor (beta-NGF), and tissue inhibitor of metalloproteinase-1 (TIMP-1) were observed in the CsA-treated group compared to controls.
Conclusions:
- Elevated levels of LIX, MCP-1, beta-NGF, and TIMP-1 are implicated as contributing factors in CsA-induced nephropathy.
- These findings highlight specific cytokines as potential targets for managing CsA-related kidney toxicity.