Proinflammatory role of angiotensin II in a rat nephrosis model induced by adriamycin
| Autor: | Adriana Pedreañez, Jaimar Rincon, Juan Pablo Hernández-Fonseca, Jesús Mosquera, Ninoska Viera, Maydelin Muñoz |
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| Rok vydání: | 2011 |
| Předmět: |
Male
Medicine (General) medicine.medical_specialty Time Factors Nephrosis Fluorescent Antibody Technique Kidney Weight Gain Losartan Proinflammatory cytokine Rats Sprague-Dawley R5-920 Endocrinology Internal medicine Internal Medicine medicine Animals Receptor Triglycerides Inflammation Angiotensin II receptor type 1 Endothelin-1 business.industry Angiotensin II Glomerulosclerosis medicine.disease Rats Disease Models Animal Proteinuria Cholesterol Doxorubicin Inflammation Mediators business Nephrotic syndrome medicine.drug |
| Zdroj: | Journal of the Renin-Angiotensin-Aldosterone System, Vol 12 (2011) |
| ISSN: | 1752-8976 1470-3203 |
| Popis: | Introduction: Nephrotic syndrome induced by adriamycin (ADR) is an experimental model of glomerulosclerosis in humans. The AT1receptor for angiotensin II (Ang II) is involved in the renal expression of the nuclear factor-kappa B (NF-ΚB) during this nephrosis. NF-ΚB is a transcription factor for proinflammatory effects of Ang II; however, there is no information about the role of this receptor in the renal proinflammatory events in ADR nephrosis.Materials and methods: To determine the role of Ang II in ADR nephrosis, Sprague-Dawley rats were treated with ADR (6 mg/kg iv). One ADR group received oral losartan treatment (15 mg/kg gavage) 3 days before ADR injection and then daily for 4 weeks, and the other group water. Animals were sacrificed at week 4 and renal macrophage infiltration, ICAM-1, superoxide anion (O2-) and Ang II expressions were analysed by indirect immunofluorescence and histochemical techniques.Results: ADR rats showed increased expression of ICAM-1, Ang II, O2-and macrophage infiltration, events that were diminished by losartan treatment. Ang II expression remained unaltered after antagonist treatment. Proteinuria was reduced after 3 weeks of treatment.Conclusions: These data suggest that Ang II plays a role in the inflammatory events during ADR-induced nephrosis, probably mediated by AT1receptors. |
| Databáze: | OpenAIRE |
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