PMID- 29046057
OWN - NLM
STAT- MEDLINE
DCOM- 20181113
LR  - 20211204
IS  - 2038-8306 (Electronic)
IS  - 1121-760X (Print)
IS  - 1121-760X (Linking)
VI  - 61
IP  - 3
DP  - 2017 Sep 13
TI  - Bile duct ligature in young rats: A revisited animal model for biliary atresia.
PG  - 2803
LID - 10.4081/ejh.2017.2803 [doi]
LID - 2803
AB  - Biliary atresia leads to cirrhosis in the vast majority of patients and 
      constitutes the first cause of paediatric liver transplantation. Animal models 
      allow us to understand the molecular basis and natural history of diseases. The 
      aim of this study is to describe a surgically created animal model of biliary 
      atresia with emphasis in long-term liver function. Forty-two 3-week-old 
      Sprague-Dawley rats were randomly divided into two groups: bile duct ligature 
      (BDL) and control. The animals were sacrificed on the 2nd, 4th, and 6th 
      postoperative weeks. Blood samples were collected for liver function analysis. 
      The spleen to body weight ratio was determined. Histopathological examination of 
      liver tissue was performed by hematoxylin-eosin and Sirius red staining. Collagen 
      quantification was determined by using colorimetric digital image analysis and 
      was expressed as a percentage of total liver tissue area. Quantitative real-time 
      polymerase chain reaction was performed to analyse gene expression levels of 
      transforming growth factor-beta1 (Tgfb1) and apeline (Apln) genes. Statistical 
      analysis was performed where P<0.05 was considered significant. Animals from 
      BDL group developed increasing cholestasis with clinical and laboratory features. 
      Splenomegaly was detected at 4th and 6th week (P<0.05). Histological 
      evaluation of the liver showed ductular reaction, portal fibrosis and bile plugs. 
      Collagen area to total liver tissue area had a median of 2.5% in the control 
      group and 6.5 %, 14.3 % and 37.7 % in BDL rats at 2nd, 4th and 6th weeks 
      respectively (P<0.001). Tgfb1 mRNA expression level was significantly higher 
      at 6th week (P<0.001) in BDL group when compared to control. Apln mRNA 
      expression level was significantly higher at 4th and 6th week (P<0.001) and 
      showed a positive linear correlation (r = 0.975, P<0.05) in BDL group when 
      compared to control. Bile duct ligature in young rats is an animal model that 
      recreates clinical, laboratory, histological and molecular findings of biliary 
      atresia. Bile duct ligature constitutes a good animal model to investigate 
      therapeutic approaches for modifying the progression of liver fibrosis in biliary 
      atresia.
FAU - Garrido, Matias
AU  - Garrido M
AD  - Universidad de Valparaiso, Centro de Investigaciones Biomedicas. 
      matias.raul@gmail.com.
FAU - Escobar, Camila
AU  - Escobar C
FAU - Zamora, Constanza
AU  - Zamora C
FAU - Rejas, Carolina
AU  - Rejas C
FAU - Varas, Juan
AU  - Varas J
FAU - Parraga, Mario
AU  - Parraga M
FAU - San Martin, Sebastian
AU  - San Martin S
FAU - Montedonico, Sandra
AU  - Montedonico S
LA  - eng
PT  - Journal Article
DEP - 20170913
PL  - Italy
TA  - Eur J Histochem
JT  - European journal of histochemistry : EJH
JID - 9207930
RN  - 0 (Amyloid)
RN  - 0 (Carrier Proteins)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (ODAM protein, human)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 9007-34-5 (Collagen)
SB  - IM
MH  - Amyloid
MH  - Animals
MH  - *Bile Ducts/pathology/surgery
MH  - Biliary Atresia/*pathology
MH  - Carrier Proteins/genetics/metabolism
MH  - Collagen/genetics/metabolism
MH  - *Disease Models, Animal
MH  - Gene Expression Regulation
MH  - Intracellular Signaling Peptides and Proteins
MH  - Ligation
MH  - Liver/pathology
MH  - Neoplasm Proteins
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Spleen/pathology
MH  - Transforming Growth Factor beta1/metabolism
PMC - PMC5607851
EDAT- 2017/10/20 06:00
MHDA- 2018/11/14 06:00
PMCR- 2017/09/18
CRDT- 2017/10/20 06:00
PHST- 2017/05/02 00:00 [received]
PHST- 2017/08/01 00:00 [accepted]
PHST- 2017/08/01 00:00 [revised]
PHST- 2017/10/20 06:00 [entrez]
PHST- 2017/10/20 06:00 [pubmed]
PHST- 2018/11/14 06:00 [medline]
PHST- 2017/09/18 00:00 [pmc-release]
AID - 10.4081/ejh.2017.2803 [doi]
PST - epublish
SO  - Eur J Histochem. 2017 Sep 13;61(3):2803. doi: 10.4081/ejh.2017.2803.