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dc.contributor.author
Toblli, Jorge Eduardo  
dc.contributor.author
Cao, Gabriel Fernando  
dc.contributor.author
Casas, Gabriel  
dc.contributor.author
Stella, Inés  
dc.contributor.author
Inserra, Pablo Ignacio Felipe  
dc.contributor.author
Angerosa, Margarita  
dc.date.available
2024-09-17T11:08:58Z  
dc.date.issued
2005-04  
dc.identifier.citation
Toblli, Jorge Eduardo; Cao, Gabriel Fernando; Casas, Gabriel; Stella, Inés; Inserra, Pablo Ignacio Felipe; et al.; NF-κB and chemokine-cytokine expression in renal tubulointerstitium in experimental hyperoxaluria. Role of the renin-angiotensin system; Springer; Urological Research; 33; 5; 4-2005; 358-367  
dc.identifier.issn
0300-5623  
dc.identifier.uri
http://hdl.handle.net/11336/244407  
dc.description.abstract
Recent evidence indicates that the reninangiotensin system (RAS) seems to play a considerable role in the development of tubulointerstitial (TI) lesions caused by hyperoxaluria (Hox). The purpose of the present study was to evaluate the specific mechanism by which Hox involving RAS induces chemokine and cytokine expression and, therefore, renal TI damage in the ethylene-glycol (ETG) induced hyperoxaluric rat model. Sprague-Dawley rats, separated into five groups, received: G1 regular water, and G2, G3, G4 and G5 1% ETG (a precursor for oxalates) in their drinking water for 4 weeks. An angiotensin converting enzyme inhibitor, benazepril (BZ) 10 mg/kg/day, angiotensin II receptor antagonists, subtype 1 (AT1) losartan (LOS) 40 mg/kg/day and subtype 2 (AT2) PD 123,319 (PD) 10 mg/kg/day, were administered daily to G3, G4 and G5, respectively. At the end of the study, the inflammatory response to Hox was evaluated using antiNF-jB (p50), anti-IL-6, anti-MCP-1; anti-RANTES and anti-ED1 (monocytes/macrophages) in each group. In spite of the same urine oxalate levels, rats belonging to the hyperoxaluric groups treated with either BZ or LOS showed significantly (P<0.01) less TI lesions together with a lower immunoexpression of inflammatory mediators when compared with untreated hyperoxaluric animals. NF-jB (p50) was increased in tubular cells in the ETG group (43.6±8.7 positive cells/mm2 ) and was significantly (P<0.01) reduced by LOS (11.2±4 positive cells/mm2 ) and even more by BZ (6.1±2.4 positive cells/ mm2 ). There was a significant (P<0.01) correlation between NF-jB (p50) positive cells and ED1 cells in the ETG group (r=0.88) and in the ETG+LOS group (r=0.92). LOS showed better control on IL-6 and MCP1 with respect to untreated rats, while BZ showed the best control on RANTES and ED1 cells in comparison with untreated animals. Renal function was significantly (P<0.01) better preserved in BZ and LOS treated groups compared to both untreated animals and rats with PD, as indicated by creatinine clearance values. These results suggest that Hox stimulates the NF-jB cascade and, therefore, induces the overexpression of inflammatory mediators like IL-6, MCP-1, and RANTES. This pathway seems to be mediated not only by AT1 but also by AT2 receptors of angiotensin II.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
Springer  
dc.rights
info:eu-repo/semantics/restrictedAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
Angiotensin II  
dc.subject
Tubulointerstitial lesion  
dc.subject
Calcium oxalate crystals  
dc.subject.classification
Ciencias y Servicios de Cuidado de la Salud  
dc.subject.classification
Ciencias de la Salud  
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
NF-κB and chemokine-cytokine expression in renal tubulointerstitium in experimental hyperoxaluria. Role of the renin-angiotensin system  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2024-09-13T11:34:31Z  
dc.journal.volume
33  
dc.journal.number
5  
dc.journal.pagination
358-367  
dc.journal.pais
Alemania  
dc.description.fil
Fil: Toblli, Jorge Eduardo. Hospital Alemán; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina  
dc.description.fil
Fil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina  
dc.description.fil
Fil: Casas, Gabriel. Hospital Alemán; Argentina  
dc.description.fil
Fil: Stella, Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina  
dc.description.fil
Fil: Inserra, Pablo Ignacio Felipe. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina  
dc.description.fil
Fil: Angerosa, Margarita. Hospital Alemán; Argentina  
dc.journal.title
Urological Research  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s00240-005-0484-4  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s00240-005-0484-4