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Article: Additive effect of PPAR-γ agonist and ARB in treatment of experimental IgA nephropathy

TitleAdditive effect of PPAR-γ agonist and ARB in treatment of experimental IgA nephropathy
Authors
KeywordsAngiotensin receptor blocker
IgA nephropathy
Nephrectomy
Peroxisome proliferator-activated receptor-γ agonist
Tubular atrophy
Issue Date2011
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00467/index.htm
Citation
Pediatric Nephrology, 2011, v. 26 n. 2, p. 257-266 How to Cite?
AbstractOur recent in vitro study demonstrated peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist potentiated the anti-inflammatory effect of angiotensin receptor blocker (ARB) in tubular epithelial cell under milieu mimicking IgA nephropathy (IgAN). Here we studied the therapeutic effect of combining a PPAR-γ agonist, rosiglitazone (Ros), with an ARB, losartan (Los), in experimental IgAN induced in Lewis rats by oral and intravenous immunization with bovine gamma-globulin (BGG). The rats were randomly divided into six groups: control, IgAN, IgAN with unilateral nephrectomy (IgAN/1K), and IgAN/1K receiving Ros, Los, or Ros + Los. Medication was given 1 week after nephrectomy until killing. Rats developing IgAN had hematuria, mesangial hypercellularity with IgA deposition, glomerular damage, and tubulointerstitial infiltration of CD25+ leukocytes accompanied by increased renal expression of TGF-β, AngII receptor subtype-1 (ATR1) and ICAM-1. The renal histopathology, albuminuria, and renal expression of TGF-β, ATR1 and ICAM-1 worsened with unilateral nephrectomy. Ros or Los reduced the renal expression of PCNA, TGF-β, ATR1, and ICAM-1 in IgAN rats with nephrectomy. Despite no difference between rats treated with monotherapy, combined therapy offered additive effect with decreased renal expression of TGF-β, ATR1 and ICAM-1 and attenuation of renal injury. Our animal study suggests combined PPAR-γ agonist and ARB holds promise for future therapy for IgAN. © 2010 IPNA.
Persistent Identifierhttp://hdl.handle.net/10722/137413
ISSN
2015 Impact Factor: 2.338
2015 SCImago Journal Rankings: 0.959
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong KongHKU 7669/08 M
L & T Charitable Foundation
House of INDOCAFE
Funding Information:

This study is supported by a General Research Fund of the Research Grants Council (Grant number: HKU 7669/08 M) of Hong Kong. Dr. L.Y. Chan was supported by the L & T Charitable Foundation and the House of INDOCAFE.

References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorGuo, Hen_HK
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLeung, JCKen_HK
dc.date.accessioned2011-08-26T14:24:33Z-
dc.date.available2011-08-26T14:24:33Z-
dc.date.issued2011en_HK
dc.identifier.citationPediatric Nephrology, 2011, v. 26 n. 2, p. 257-266en_HK
dc.identifier.issn0931-041Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/137413-
dc.description.abstractOur recent in vitro study demonstrated peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist potentiated the anti-inflammatory effect of angiotensin receptor blocker (ARB) in tubular epithelial cell under milieu mimicking IgA nephropathy (IgAN). Here we studied the therapeutic effect of combining a PPAR-γ agonist, rosiglitazone (Ros), with an ARB, losartan (Los), in experimental IgAN induced in Lewis rats by oral and intravenous immunization with bovine gamma-globulin (BGG). The rats were randomly divided into six groups: control, IgAN, IgAN with unilateral nephrectomy (IgAN/1K), and IgAN/1K receiving Ros, Los, or Ros + Los. Medication was given 1 week after nephrectomy until killing. Rats developing IgAN had hematuria, mesangial hypercellularity with IgA deposition, glomerular damage, and tubulointerstitial infiltration of CD25+ leukocytes accompanied by increased renal expression of TGF-β, AngII receptor subtype-1 (ATR1) and ICAM-1. The renal histopathology, albuminuria, and renal expression of TGF-β, ATR1 and ICAM-1 worsened with unilateral nephrectomy. Ros or Los reduced the renal expression of PCNA, TGF-β, ATR1, and ICAM-1 in IgAN rats with nephrectomy. Despite no difference between rats treated with monotherapy, combined therapy offered additive effect with decreased renal expression of TGF-β, ATR1 and ICAM-1 and attenuation of renal injury. Our animal study suggests combined PPAR-γ agonist and ARB holds promise for future therapy for IgAN. © 2010 IPNA.en_HK
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00467/index.htmen_HK
dc.relation.ispartofPediatric Nephrologyen_HK
dc.rightsThe original publication is available at www.springerlink.com-
dc.subjectAngiotensin receptor blockeren_HK
dc.subjectIgA nephropathyen_HK
dc.subjectNephrectomyen_HK
dc.subjectPeroxisome proliferator-activated receptor-γ agonisten_HK
dc.subjectTubular atrophyen_HK
dc.subject.meshAngiotensin II Type 1 Receptor Blockers - pharmacology - therapeutic use-
dc.subject.meshGlomerulonephritis, IGA - chemically induced - drug therapy - metabolism - pathology-
dc.subject.meshLosartan - pharmacology - therapeutic use-
dc.subject.meshPPAR gamma - agonists-
dc.subject.meshThiazolidinediones - pharmacology - therapeutic use-
dc.titleAdditive effect of PPAR-γ agonist and ARB in treatment of experimental IgA nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00467-010-1703-yen_HK
dc.identifier.pmid21125406-
dc.identifier.scopuseid_2-s2.0-78751581941en_HK
dc.identifier.hkuros190908en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78751581941&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issue2en_HK
dc.identifier.spage257en_HK
dc.identifier.epage266en_HK
dc.identifier.isiWOS:000286791600012-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridChan, LYY=55182644100en_HK
dc.identifier.scopusauthoridGuo, H=55468645700en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.citeulike8387011-

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