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Dipeptidyl peptidase IV inhibitor attenuates kidney injury in rat remnant kidney
DC Field | Value | Language |
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dc.contributor.author | Joo, Kwon Wook | - |
dc.contributor.author | Kim, Sejoong | - |
dc.contributor.author | Ahn, Shin-young | - |
dc.contributor.author | Chin, Ho Jun | - |
dc.contributor.author | Chae, Dong-Wan | - |
dc.contributor.author | Lee, Jeonghwan | - |
dc.contributor.author | Han, Jin Suk | - |
dc.contributor.author | Na, Ki Young | - |
dc.date.accessioned | 2013-05-31T00:56:50Z | - |
dc.date.available | 2013-05-31T00:56:50Z | - |
dc.date.issued | 2013-04-27 | - |
dc.identifier.citation | BMC Nephrology, vol.14 no.98 | ko_KR |
dc.identifier.issn | 1471-2369 | - |
dc.identifier.uri | http://www.biomedcentral.com/1471-2369/14/98 | - |
dc.identifier.uri | https://hdl.handle.net/10371/82535 | - |
dc.description.abstract | Background : The inhibition of dipeptidyl peptidase (DPP) IV shows protective effects on tissue injury of the heart, lung, and kidney. Forkhead box O (FoxO) transcriptional factors regulate cellular differentiation, growth, survival, the cell cycle, metabolism, and oxidative stress. The aims of this study were to investigate whether the DPP IV inhibitor sitagliptin could attenuate kidney injury and to evaluate the status of FoxO3a signaling in the rat remnant kidney model.
Methods : Rats were received two-step surgery of 5/6 renal mass reduction and fed on an oral dose of 200 mg/kg/day sitagliptin for 8 weeks. Before and after the administration of sitagliptin, physiologic parameters were measured. After 8 weeks of treatment, the kidneys were harvested. Results : The sitagliptin treatment attenuated renal dysfunction. A histological evaluation revealed that glomerulosclerosis and tubulointerstitial injury were significantly decreased by sitagliptin. Sitagliptin decreased DPP IV activity and increased the renal expression of glucagon-like peptide-1 receptor (GLP-1R). The subtotal nephrectomy led to the activation of phosphatidylinositol 3-kinase (PI3K)-Akt and FoxO3a phosphorylation, whereas sitagliptin treatment reversed these changes, resulting in PI3K-Akt pathway inactivation and FoxO3a dephosphorylation. The renal expression of catalase was increased and the phosphorylation of c-Jun N-terminal kinase (JNK) was decreased by sitagliptin. Sitagliptin treatment reduced apoptosis by decreasing cleaved caspase-3 and −9 and Bax levels and decreased macrophage infiltration. Conclusions : In rat remnant kidneys, DPP IV inhibitor attenuated renal dysfunction and structural damage. A reduction of apoptosis, inflammation and an increase of antioxidant could be suggested as a renoprotective mechanism together with the activation of FoxO3a signaling. Therefore, DPP IV inhibitors might provide a promising approach for treating CKD, but their application in clinical practice remains to be investigated. | ko_KR |
dc.description.sponsorship | This study was supported by the Seoul National University Bundang Hospital [Grant 06-2012-091 and 02-2011-013]. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BioMed Central | - |
dc.subject | Dipeptidyl peptidase IV | ko_KR |
dc.subject | Glucagon-like peptide-1 receptor | ko_KR |
dc.subject | FoxO3a | ko_KR |
dc.subject | Sitagliptin | ko_KR |
dc.subject | Kidney injury | ko_KR |
dc.title | Dipeptidyl peptidase IV inhibitor attenuates kidney injury in rat remnant kidney | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 주권욱 | - |
dc.contributor.AlternativeAuthor | 김세중 | - |
dc.contributor.AlternativeAuthor | 안신영 | - |
dc.contributor.AlternativeAuthor | 채동완 | - |
dc.contributor.AlternativeAuthor | 이정환 | - |
dc.contributor.AlternativeAuthor | 한진석 | - |
dc.contributor.AlternativeAuthor | 나기영 | - |
dc.contributor.AlternativeAuthor | 진호준 | - |
dc.identifier.doi | 10.1186/1471-2369-14-98 | - |
dc.language.rfc3066 | en | - |
dc.description.version | Peer Reviewed | - |
dc.rights.holder | Kwon Wook Joo et al.; licensee BioMed Central Ltd. | - |
dc.date.updated | 2013-05-08T03:11:01Z | - |
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