Previous exposure to cigarette smoke aggravates experimental cyclosporine-induced nephrotoxicity
| Autor: | Gloria E. Mendes, Rael L Matimoto, Terezila Machado Coimbra, Sandra M Oliveira, Emmanuel A. Burdmann, Marcus A.M. Luz, Rafael P S Souza, Carla Patrícia Carlos, Sueli A Alves |
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| Rok vydání: | 2012 |
| Předmět: |
Male
medicine.medical_specialty Renal function Hematocrit Pharmacology Kidney Nephrotoxicity chemistry.chemical_compound Internal medicine MODELOS ANIMAIS DE DOENÇAS medicine Animals Humans Vimentin Rats Wistar medicine.diagnostic_test business.industry Nitrotyrosine Smoking Hemodynamics Kidney metabolism Drug Synergism Fibrosis Actins Rats Disease Models Animal medicine.anatomical_structure Endocrinology chemistry Nephrology Renal blood flow Vascular resistance Tubulointerstitial fibrosis Cyclosporine Nephritis Interstitial Tyrosine business Immunosuppressive Agents Glomerular Filtration Rate |
| Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
| ISSN: | 1421-9670 |
| Popis: | Background/Aims: The effects of cigarette smoke (CS) on cyclosporine (CsA)-induced nephrotoxicity are poorly studied. This study aims to assess the effects of previous exposure to CS on CsA nephrotoxicity. Methods: Rats were either exposed to CS or sham (S) procedures for 10 min twice a day for 20 weeks. From the 16th to the 20th week, they received a low-salt diet. Beginning with the 17th week, they were given 2.5 mg/day CsA or vehicle (VH) for 3 weeks. The final groups were VH/CS, CsA/CS, VH/S, and CsA/S. On day 141, glomerular filtration rate (GFR), renal blood flow (RBF), renal vascular resistance (RVR), tubulointerstitial fibrosis, and CsA blood levels were measured and immunohistochemistry was analyzed for renal α-smooth muscle actin (SMA), nitrotyrosine, and vimentin. Results: CsA decrease in GFR was enhanced by CS exposure. CsA associated with CS induced higher periglomerular α-SMA and renal nitrotyrosine expression. CsA decreased RBF, but increased RVR, tubulointerstitial fibrosis, and α-SMA and renal vimentin expression. These changes and the CsA blood levels were not affected by CS exposure. Conclusion: CS aggravated the CsA-induced impairment of GFR and CS associated with CsA caused the development of periglomerular structural lesions and oxidative stress in a rat model of CsA nephrotoxicity. |
| Databáze: | OpenAIRE |
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