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Article: Rosiglitazone protects diabetic rats against kidney disease through the suppression of renal moncyte chemoattractant protein-1 expression

TitleRosiglitazone protects diabetic rats against kidney disease through the suppression of renal moncyte chemoattractant protein-1 expression
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2009
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jdiacomp
Citation
Journal of Diabetes and its Complications, 2009, v. 23 n. 2, p. 124-129 How to Cite?
Abstract
Although the pathogenetic mechanisms of diabetic nephropathy (DN) have not been elucidated thoroughly, an inflammatory mechanism has been suggested to contribute to its development and progression. Moncyte chemoattractant protein (MCP)-1 is a chemokine that can attract macrophages and T cells from the circulation to the local kidney, then activate them, and ultimately injure the renal tissue. Recent studies have demonstrated that thiazolidinediones decrease urinary albumin (ALB) excretion, which may be partly related to its anti-inflammatory action. Therefore, the effects of rosiglitazone on renal inflammation and renal injury were investigated in streptozotocin (STZ)-induced diabetic rats in this study. We examined the urinary excretion rates of ALB, retinal-binding protein (RBP), and MCP-1 of normal control group (Group C, n=8), STZ-induced diabetes mellitus group (Group D, n=8), and diabetes plus rosiglitazone (5 mg{dot operator}kg-1{dot operator}day-1) treatment group (Group R, n=8) at the eighth week. The renal tissues of diabetic rats were obtained for reverse transcriptase-polymerase chain reaction to examine the expression of MCP-1 mRNA. Our results showed that compared to normal control, urinary excretion rates of ALB, RBP, and MCP-1 were significantly increased in untreated diabetic rats at the eighth week. However, rosiglitazone treatment could markedly decrease all the parameters above. In addition, urinary excretion rate of MCP-1 showed positive correlations with urinary ALB excretion, urinary RBP excretion, and kidney/body weight. The expressions of MCP-1 mRNA in renal tissues were markedly up-regulated in untreated diabetic rats, and these could be notably reduced by rosiglitazone treatment. In conclusion, rosiglitazone may have a potential therapeutic target in DN, which may be partly attributed to lowering of the expression of MCP-1 in the local kidney and the urinary excretion of MCP-1. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/92171
ISSN
2013 Impact Factor: 1.925
ISI Accession Number ID
Funding AgencyGrant Number
Basic Research Program of the Science & Engineering Foundation of Anhui Education Bureau of China2006KJ318B
Nature Science Foundation of Anhui Province of China070413255X
Funding Information:

This work was supported by Grant 2006KJ318B from the Basic Research Program of the Science & Engineering Foundation of Anhui Education Bureau of China and Grant 070413255X from the Nature Science Foundation of Anhui Province of China.

References

 

Author Affiliations
  1. Anhui Medical University
  2. Anhui Provincial Hospital
  3. Anhui Medical College
DC FieldValueLanguage
dc.contributor.authorZheng, Men_HK
dc.contributor.authorYe, Sen_HK
dc.contributor.authorZhai, Zen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorLi, Xen_HK
dc.contributor.authorYang, Gen_HK
dc.contributor.authorFan, Aen_HK
dc.contributor.authorWang, Yen_HK
dc.date.accessioned2010-09-17T10:38:10Z-
dc.date.available2010-09-17T10:38:10Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal of Diabetes and its Complications, 2009, v. 23 n. 2, p. 124-129en_HK
dc.identifier.issn1056-8727en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92171-
dc.description.abstractAlthough the pathogenetic mechanisms of diabetic nephropathy (DN) have not been elucidated thoroughly, an inflammatory mechanism has been suggested to contribute to its development and progression. Moncyte chemoattractant protein (MCP)-1 is a chemokine that can attract macrophages and T cells from the circulation to the local kidney, then activate them, and ultimately injure the renal tissue. Recent studies have demonstrated that thiazolidinediones decrease urinary albumin (ALB) excretion, which may be partly related to its anti-inflammatory action. Therefore, the effects of rosiglitazone on renal inflammation and renal injury were investigated in streptozotocin (STZ)-induced diabetic rats in this study. We examined the urinary excretion rates of ALB, retinal-binding protein (RBP), and MCP-1 of normal control group (Group C, n=8), STZ-induced diabetes mellitus group (Group D, n=8), and diabetes plus rosiglitazone (5 mg{dot operator}kg-1{dot operator}day-1) treatment group (Group R, n=8) at the eighth week. The renal tissues of diabetic rats were obtained for reverse transcriptase-polymerase chain reaction to examine the expression of MCP-1 mRNA. Our results showed that compared to normal control, urinary excretion rates of ALB, RBP, and MCP-1 were significantly increased in untreated diabetic rats at the eighth week. However, rosiglitazone treatment could markedly decrease all the parameters above. In addition, urinary excretion rate of MCP-1 showed positive correlations with urinary ALB excretion, urinary RBP excretion, and kidney/body weight. The expressions of MCP-1 mRNA in renal tissues were markedly up-regulated in untreated diabetic rats, and these could be notably reduced by rosiglitazone treatment. In conclusion, rosiglitazone may have a potential therapeutic target in DN, which may be partly attributed to lowering of the expression of MCP-1 in the local kidney and the urinary excretion of MCP-1. © 2009 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jdiacompen_HK
dc.relation.ispartofJournal of Diabetes and its Complicationsen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleRosiglitazone protects diabetic rats against kidney disease through the suppression of renal moncyte chemoattractant protein-1 expressionen_HK
dc.typeArticleen_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp1318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jdiacomp.2007.11.012en_HK
dc.identifier.pmid18413206-
dc.identifier.scopuseid_2-s2.0-60049086525en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-60049086525&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue2en_HK
dc.identifier.spage124en_HK
dc.identifier.epage129en_HK
dc.identifier.isiWOS:000263887300008-
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