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Effects of mycophenolate mofetil on cisplatin-induced renal dysfunction in rats
Sherif Y Saad1, Maha M Arafah, Tawfeeg A Najjar
1Department of Clinical Pharmacy, College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh, 11451, Saudi Arabia. sherifibrahem@yahoo.co.uk
Purpose:
Inflammation and oxidative stress are important events among the plethora of mechanisms involved in cisplatin (CDDP)-induced nephrotoxicity. The aim of this study was to evaluate the effect of mycophenolate mofetil (MMF), an immunosuppressive, in the protection against CDDP-induced renal dysfunction.
Methods:
Rats were divided into four groups; untreated-control group, CDDP-treated group (7 mg/kg, single intraperitoneal dose), MMF-treated group (40 mg/kg/day orally for 5 successive days) and the fourth group was treated with both drugs and MMF treatment was started 1 day prior to CDDP administration. Nephrotoxicity was assessed 7 days after the CDDP treatment by measuring serum indices of nephrotoxicity, kidney weight as a percentage of total body weight, kidney's tissue peroxidative alterations and total nitrate/nitrite concentration (NOx) and the results were confirmed histopathologically.
Results:
Rats treated with CDDP showed marked nephrotoxicity as evidenced from the significant increase in serum creatinine and urea levels and decrease in serum calcium and albumin levels. Kidneys of CDDP-treated rats showed significant increases in kidney weight and malondialdehyde (MDA) production level and decreases in total NOx concentration, glutathione peroxidase (GPx) activity and reduced glutathione (GSH) content levels. Histopathological assessment of kidneys of CDDP-treated rats revealed extensive tubular necrosis with "sloughing off" of the renal tubular lining cells, intratubular hyaline casts and mononuclear cell infiltration. Treatment with MMF significantly protected the rats against CDDP-induced nephrotoxicity. The rise in serum creatinine and urea levels, kidney weight and kidney tissue MDA production, depletion of "endogenous antioxidant reserve" including GPx activity and reduced GSH content levels and the deleterious histopathological changes induced by CDDP treatment were significantly mitigated by MMF treatment.
Conclusions:
MMF treatment dramatically ameliorates CDDP-induced renal dysfunction.
Insights
Mycophenolate mofetil (MMF) significantly protects against cisplatin (CDDP)-induced kidney damage. MMF treatment mitigates markers of nephrotoxicity and improves kidney function in rats exposed to CDDP.
Area of Science:
- Nephrology
- Pharmacology
- Toxicology
Background:
- Cisplatin (CDDP) is a potent chemotherapeutic agent with significant nephrotoxicity.
- Inflammation and oxidative stress are key mechanisms underlying CDDP-induced kidney damage.
Purpose of the Study:
- To investigate the protective effects of mycophenolate mofetil (MMF) against cisplatin-induced nephrotoxicity.
- To evaluate MMF's impact on renal dysfunction caused by CDDP.
Main Methods:
- Rats were administered CDDP and/or MMF, with MMF treatment preceding CDDP in combination groups.
- Nephrotoxicity was assessed via serum markers (creatinine, urea, calcium, albumin), kidney weight, oxidative stress indicators (MDA, NOx), and histopathology.
Main Results:
- CDDP treatment led to significant increases in serum creatinine and urea, elevated kidney weight and MDA, and reduced antioxidant levels (GPx, GSH).
- Histopathology confirmed severe tubular necrosis and inflammation in CDDP-treated rats.
- MMF treatment significantly counteracted these CDDP-induced changes, preserving kidney function and structure.
Conclusions:
- Mycophenolate mofetil (MMF) demonstrates potent protective effects against cisplatin (CDDP)-induced nephrotoxicity.
- MMF ameliorates renal dysfunction by reducing oxidative stress and inflammation associated with CDDP treatment.
