N-Acetyl-seryl-aspartyl-lysyl-proline Alleviates Renal Fibrosis Induced by Unilateral Ureteric Obstruction in BALB/C Mice
To expand the armamentarium of treatment for chronic kidney disease (CKD), we explored the utility of boosting endogenously synthesized N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is augmented by inhibition of the angiotensin converting enzyme. Male BALB/c mice underwent unilateral ureter...
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Published in | Mediators of Inflammation Vol. 2015; no. 2015; pp. 99 - 108-109 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
Hindawi Limiteds
01.01.2015
Hindawi Publishing Corporation John Wiley & Sons, Inc Hindawi Limited |
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Abstract | To expand the armamentarium of treatment for chronic kidney disease (CKD), we explored the utility of boosting endogenously synthesized N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is augmented by inhibition of the angiotensin converting enzyme. Male BALB/c mice underwent unilateral ureteral ligation (UUO) or sham operation and received exogenously administered Ac-SDKP delivered via a subcutaneous osmotic minipump or Captopril treatment by oral gavage. Seven days after UUO, there were significant reductions in the expression of both collagen 1 and collagen 3 in kidneys treated with Ac-SDKP or Captopril, and there was a trend towards reductions in collagen IV, α-SMA, and MCP-1 versus control. However, no significant attenuation of interstitial injury or macrophage infiltration was observed. These findings are in contrary to observations in other models and underscore the fact that a longer treatment time frame may be required to yield anti-inflammatory effects in BALB/c mice treated with Ac-SDKP compared to untreated mice. Finding an effective treatment regimen for CKD requires fine-tuning of pharmacologic protocols. |
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AbstractList | To expand the armamentarium of treatment for chronic kidney disease (CKD), we explored the utility of boosting endogenously synthesized N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is augmented by inhibition of the angiotensin converting enzyme. Male BALB/c mice underwent unilateral ureteral ligation (UUO) or sham operation and received exogenously administered Ac-SDKP delivered via a subcutaneous osmotic minipump or Captopril treatment by oral gavage. Seven days after UUO, there were significant reductions in the expression of both collagen 1 and collagen 3 in kidneys treated with Ac-SDKP or Captopril, and there was a trend towards reductions in collagen IV, α-SMA, and MCP-1 versus control. However, no significant attenuation of interstitial injury or macrophage infiltration was observed. These findings are in contrary to observations in other models and underscore the fact that a longer treatment time frame may be required to yield anti-inflammatory effects in BALB/c mice treated with Ac-SDKP compared to untreated mice. Finding an effective treatment regimen for CKD requires fine-tuning of pharmacologic protocols. To expand the armamentarium of treatment for chronic kidney disease (CKD), we explored the utility of boosting endogenously synthesized N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is augmented by inhibition of the angiotensin converting enzyme. Male BALB/c mice underwent unilateral ureteral ligation (UUO) or sham operation and received exogenously administered Ac-SDKP delivered via a subcutaneous osmotic minipump or Captopril treatment by oral gavage. Seven days after UUO, there were significant reductions in the expression of both collagen 1 and collagen 3 in kidneys treated with Ac-SDKP or Captopril, and there was a trend towards reductions in collagen IV, α -SMA, and MCP-1 versus control. However, no significant attenuation of interstitial injury or macrophage infiltration was observed. These findings are in contrary to observations in other models and underscore the fact that a longer treatment time frame may be required to yield anti-inflammatory effects in BALB/c mice treated with Ac-SDKP compared to untreated mice. Finding an effective treatment regimen for CKD requires fine-tuning of pharmacologic protocols. |
Audience | Academic |
Author | Gary C. W. Chan Wai Han Yiu Miao Lin Sydney C. W. Tang Dickson W. L. Wong Xiao Ru Huang Hui Yao Lan Hao Jia Wu |
AuthorAffiliation | 1 Division of Nephrology, Department of Medicine, The University of Hong Kong, Hong Kong 2 Department of Medicine and Therapeutics and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong |
AuthorAffiliation_xml | – name: 1 Division of Nephrology, Department of Medicine, The University of Hong Kong, Hong Kong – name: 2 Department of Medicine and Therapeutics and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong |
Author_xml | – sequence: 1 fullname: Tang, Sydney C. W. – sequence: 2 fullname: Huang, Xiao Ru – sequence: 3 fullname: Lin, Miao – sequence: 4 fullname: Wong, Dickson W. L. – sequence: 5 fullname: Wu, Hao Jia – sequence: 6 fullname: Yiu, Wai Han – sequence: 7 fullname: Chan, Gary C. W. – sequence: 8 fullname: Lan, Hui Y. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26508815$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1080_14712598_2018_1473371 crossref_primary_10_1016_j_pharep_2017_03_002 crossref_primary_10_1111_1440_1681_13565 crossref_primary_10_1139_cjpp_2018_0570 crossref_primary_10_2147_JIR_S306883 crossref_primary_10_1042_CS20200923 crossref_primary_10_3390_ijms232113282 crossref_primary_10_1016_j_taap_2020_115255 crossref_primary_10_1111_nep_13000 |
Cites_doi | 10.1161/01.cir.103.25.3136 10.1681/asn.2005040385 10.1681/ASN.V13suppl_1s37 10.1097/hjh.0b013e32834103ee 10.3892/ijmm-00000527 10.1161/01.hyp.0000107777.91185.89 10.1016/0006-291x(90)90489-a 10.1038/sj.ki.5002674 10.1161/01.HYP.0000258406.66954.4f 10.1038/ki.2009.86 10.1093/ndt/gfn699 10.1111/j.1523-1755.2005.00486.x 10.1161/01.hyp.37.2.794 10.1007/s11255-013-0520-1 10.1053/j.ackd.2005.07.011 10.1681/asn.2010111210 10.1038/ki.2013.11 10.1038/labinvest.2011.81 10.1073/pnas.86.3.779 |
ContentType | Journal Article |
Copyright | Copyright © 2015 Gary C. W. Chan et al. COPYRIGHT 2015 John Wiley & Sons, Inc. Copyright © 2015 Gary C. W. Chan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2015 Gary C. W. Chan et al. 2015 |
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SubjectTerms | Actins - metabolism Angiotensin converting enzyme Angiotensin-Converting Enzyme Inhibitors - therapeutic use Animals Captopril - chemistry Chemokine CCL2 - metabolism Chronic kidney failure Collagen Type IV - metabolism Enzymes Fibrosis Fibrosis - drug therapy Gene expression Histology Immunohistochemistry Inflammation Kidney Diseases - drug therapy Kidneys Laboratory animals Lymphocytes - cytology Macrophages - cytology Macrophages - metabolism Male Mice Mice, Inbred BALB C Morphology Muscle, Smooth - metabolism Nephrology Oligopeptides - therapeutic use Physiological aspects Real-Time Polymerase Chain Reaction Rodents Studies Ureteral Obstruction - drug therapy |
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Title | N-Acetyl-seryl-aspartyl-lysyl-proline Alleviates Renal Fibrosis Induced by Unilateral Ureteric Obstruction in BALB/C Mice |
URI | https://www.airitilibrary.com/Article/Detail/P20160527003-201512-201703060008-201703060008-99-108-109 https://search.emarefa.net/detail/BIM-1072231 https://dx.doi.org/10.1155/2015/283123 https://www.ncbi.nlm.nih.gov/pubmed/26508815 https://www.proquest.com/docview/1722856020 https://search.proquest.com/docview/1728259753 https://pubmed.ncbi.nlm.nih.gov/PMC4609855 https://doaj.org/article/beaf275db73d4efba7ef1f4d6cdb73de |
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