Protective Effect of Recombinant Human Erythropoietin Against Cisplatin-Induced Oxidative Stress and Nephrotoxicity in Rat Kidney
| Autor: | Anis Belarbia, Abdelatif Achour, Hassen Bacha, Imen Ayed Boussema, Karima Rjiba-Touati |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Male
Pharmacology Kidney Toxicology medicine.disease_cause Antioxidants Blood Urea Nitrogen Nephrotoxicity Protein Carbonylation chemistry.chemical_compound Malondialdehyde Animals Anticarcinogenic Agents Humans Medicine Rats Wistar Erythropoietin Blood urea nitrogen Creatinine business.industry Kidney metabolism Glutathione Acute Kidney Injury Catalase Recombinant Proteins Rats Oxidative Stress Biochemistry chemistry Lipid Peroxidation Cisplatin business Oxidative stress medicine.drug |
| Zdroj: | International Journal of Toxicology. 30:510-517 |
| ISSN: | 1092-874X 1091-5818 |
| DOI: | 10.1177/1091581810411931 |
| Popis: | Cisplatin (Cisp) is one of the most widely used chemotherapeutic agents for the treatment of several human malignancies. The efficacy of Cisp is dose dependent and at higher doses serious kidney injury may occur. Recombinant human erythropoietin (rhEPO) has recently been shown to exert an important cytoprotective effect in experimental brain injury and ischemic acute renal failure. The aim of the present study was to explore whether rhEPO administration is protective against Cisp-induced oxidative damage and renal injury. Our results showed that Cisp induced a marked oxidative stress and renal failure. Administration of rhEPO (pre-, co- or postadministration with regard to Cisp) decreased oxidative damage induced by Cisp. Recombinant human EPO reduced malondialdehyde and protein carbonyl levels. Recombinant human EPO also prevented glutathione depletion and ameliorated the increased catalase activity induced by Cisp treatment. Furthermore, rhEPO restored creatinine and blood urea nitrogen levels increased by Cisp. We concluded that rhEPO administration especially in pretreatment condition protected rats against Cisp-induced renal oxidative stress and nephrotoxicity. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|