PMID- 21042772
OWN - NLM
STAT- MEDLINE
DCOM- 20110308
LR  - 20190606
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 26
IP  - 6
DP  - 2010 Dec
TI  - N-acetyl-seryl-aspartyl-lysyl-proline attenuates renal inflammation and 
      tubulointerstitial fibrosis in rats.
PG  - 795-801
AB  - It has been reported that N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) 
      attenuates renal and cardiac inflammation as well as fibrosis in hypertensive 
      rats. In this study, we investigated these effects using a unilateral ureteral 
      obstruction (UUO) model. Eighteen male Wistar rats were randomly divided into 
      three groups: control, UUO/vehicle and UUO/Ac-SDKP groups. Animal models of renal 
      inflammation and tubulointerstitial fibrosis were established with unilateral 
      ureteral ligation in rats. Ac-SDKP and vehicle were infused subcutaneously by 
      using osmotic mini pumps for two weeks. On the 14th day post-injection, kidney 
      histological changes of each group were observed by hematoxylin-eosin and 
      Masson's stain. Renal macrophage infiltration, together with protein expression 
      and localization of monocyte chemoattractant protein-1 (MCP-1), nuclear 
      factor-kappa B (NF-kappaB), alpha-smooth muscle actin (alpha-SMA) and transforming growth 
      factor-beta1 (TGF-beta1) in renal tissue was assessed by immunohistochemical staining. 
      Gene expression of MCP-1 and TGF-beta1 was analyzed with reverse 
      transcription-polymerase chain reaction. Ac-SDKP-treated animals demonstrated 
      less severe renal inflammation and tubulointerstitial fibrosis. Interstitial 
      fibrosis was significantly attenuated with Ac-SDKP. ED-1 was expressed in the 
      interstitium of the UUO/vehicle group kidneys and decreased with Ac-SDKP 
      treatment. MCP-1, NF-kappaB, alpha-SMA and TGF-beta1 were increased in the renal 
      interstitium and tubular epithelial cells of the UUO/vehicle group. Ac-SDKP 
      significantly reduced their expressions. Gene expressions of MCP-1 and TGF-beta1 
      were upregulated in the UUO/vehicle group kidneys and were significantly 
      inhibited by Ac-SDKP. In conclusion, in the rat UUO model Ac-SDKP administration 
      protected against renal inflammation and tubulointerstitial fibrosis. The 
      inhibitory effect of Ac-SDKP was mediated by the reduction in the expression of 
      MCP-1, NF-kappaB, alpha-SMA and TGF-beta1.
FAU - Wang, Mingao
AU  - Wang M
AD  - Department of Nephrology, The First Affiliated Hospital of Harbin Medical 
      University, Harbin, P.R. China.
FAU - Liu, Ruichan
AU  - Liu R
FAU - Jia, Xibei
AU  - Jia X
FAU - Mu, Suhong
AU  - Mu S
FAU - Xie, Rujuan
AU  - Xie R
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Biomarkers)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Oligopeptides)
RN  - H041538E9P (goralatide)
SB  - IM
MH  - Animals
MH  - Biomarkers/metabolism
MH  - Disease Models, Animal
MH  - Fibrosis/*drug therapy/metabolism/pathology
MH  - Histocytochemistry
MH  - Intercellular Signaling Peptides and Proteins/genetics/metabolism
MH  - Kidney Tubules/*pathology
MH  - Macrophages/metabolism
MH  - Male
MH  - Nephritis/*drug therapy/metabolism/pathology
MH  - Oligopeptides/*pharmacology
MH  - Rats
MH  - Rats, Wistar
EDAT- 2010/11/03 06:00
MHDA- 2011/03/09 06:00
CRDT- 2010/11/03 06:00
PHST- 2010/11/03 06:00 [entrez]
PHST- 2010/11/03 06:00 [pubmed]
PHST- 2011/03/09 06:00 [medline]
AID - 10.3892/ijmm_00000527 [doi]
PST - ppublish
SO  - Int J Mol Med. 2010 Dec;26(6):795-801. doi: 10.3892/ijmm_00000527.