Pioglitazone attenuates diabetic nephropathy through an anti-inflammatory mechanism in type 2 diabetic rats
DC Field | Value | Language |
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dc.contributor.author | Ko, Gang Jee | - |
dc.contributor.author | Kang, Young Sun | - |
dc.contributor.author | Han, Sang Youb | - |
dc.contributor.author | Lee, Mi Hwa | - |
dc.contributor.author | Song, Hye Kyoung | - |
dc.contributor.author | Han, Kum Hyun | - |
dc.contributor.author | Kim, Hyoung Kyu | - |
dc.contributor.author | Han, Jee Young | - |
dc.contributor.author | Cha, Dae Ryong | - |
dc.date.accessioned | 2021-09-09T04:49:35Z | - |
dc.date.available | 2021-09-09T04:49:35Z | - |
dc.date.created | 2021-06-10 | - |
dc.date.issued | 2008-09 | - |
dc.identifier.issn | 0931-0509 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/122804 | - |
dc.description.abstract | Background. Peroxisome proliferator-activated receptors (PPARs) are nuclear transcription factors that play a role in insulin sensitivity, lipid metabolism and inflammation. However, the effects of PPAR gamma agonist on renal inflammation have not been fully examined in type 2 diabetic nephropathy. Methods. In the present study, we investigated the effect and molecular mechanism of the PPAR gamma agonist, pioglitazone, on the progression of diabetic nephropathy in type 2 diabetic rats. Inflammatory markers including NF-kappa B, MCP-1 and pro-fibrotic cytokines were determined by RT-PCR, western blot, immunohistochemical staining and EMSA. In addition, to evaluate the direct anti-inflammatory effect of PPAR gamma agonist, we performed an in vitro study using mesangial cells. Results. Treatment of OLETF rats with pioglitazone improved insulin sensitivity and kidney/body weight, but had a little effect on blood pressure. Pioglitazone treatment markedly reduced urinary albumin and MCP-1 excretion, and ameliorated glomerulosclerosis. In cDNA microarray analysis using renal cortical tissues, several inflammatory and profibrotic genes were significantly down-regulated by pioglitazone including NF-kappa B, CCL2, TGF beta 1, PAI-1 and VEGF. In renal tissues, pioglitazone treatment significantly reduced macrophage infiltration and NF-kappa B activation in association with a decrease in type IV collagen, PAI-1, and TGF beta 1 expression. In cultured mesangial cells, pioglitazone-activated endogenous PPAR gamma transcriptional activity and abolished high glucose-induced collagen production. In addition, pioglitazone treatment also markedly suppressed high glucose-induced MCP-1 synthesis and NF-kappa B activation. Conclusions. These data suggest that pioglitazone not only improves insulin resistance, glycaemic control and lipid profile, but also ameliorates renal injury through an anti-inflammatory mechanism in type 2 diabetic rats. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | OXFORD UNIV PRESS | - |
dc.subject | ACTIVATED RECEPTOR-GAMMA | - |
dc.subject | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | - |
dc.subject | URINARY ALBUMIN EXCRETION | - |
dc.subject | KAPPA-B ACTIVATION | - |
dc.subject | RENAL INJURY | - |
dc.subject | ROSIGLITAZONE | - |
dc.subject | EXPRESSION | - |
dc.subject | AGONIST | - |
dc.subject | GLOMERULOSCLEROSIS | - |
dc.subject | TROGLITAZONE | - |
dc.title | Pioglitazone attenuates diabetic nephropathy through an anti-inflammatory mechanism in type 2 diabetic rats | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Ko, Gang Jee | - |
dc.contributor.affiliatedAuthor | Kang, Young Sun | - |
dc.contributor.affiliatedAuthor | Kim, Hyoung Kyu | - |
dc.contributor.affiliatedAuthor | Cha, Dae Ryong | - |
dc.identifier.doi | 10.1093/ndt/gfn157 | - |
dc.identifier.scopusid | 2-s2.0-56949105387 | - |
dc.identifier.wosid | 000259372400012 | - |
dc.identifier.bibliographicCitation | NEPHROLOGY DIALYSIS TRANSPLANTATION, v.23, no.9, pp.2750 - 2760 | - |
dc.relation.isPartOf | NEPHROLOGY DIALYSIS TRANSPLANTATION | - |
dc.citation.title | NEPHROLOGY DIALYSIS TRANSPLANTATION | - |
dc.citation.volume | 23 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 2750 | - |
dc.citation.endPage | 2760 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Transplantation | - |
dc.relation.journalResearchArea | Urology & Nephrology | - |
dc.relation.journalWebOfScienceCategory | Transplantation | - |
dc.relation.journalWebOfScienceCategory | Urology & Nephrology | - |
dc.subject.keywordPlus | ACTIVATED RECEPTOR-GAMMA | - |
dc.subject.keywordPlus | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | - |
dc.subject.keywordPlus | URINARY ALBUMIN EXCRETION | - |
dc.subject.keywordPlus | KAPPA-B ACTIVATION | - |
dc.subject.keywordPlus | RENAL INJURY | - |
dc.subject.keywordPlus | ROSIGLITAZONE | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | AGONIST | - |
dc.subject.keywordPlus | GLOMERULOSCLEROSIS | - |
dc.subject.keywordPlus | TROGLITAZONE | - |
dc.subject.keywordAuthor | diabetic nephropathy | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordAuthor | nuclear factor-kappa B | - |
dc.subject.keywordAuthor | PPAR gamma agonist | - |
dc.subject.keywordAuthor | type 2 diabetes | - |
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