Document Detail


Minimal role of hepatic transporters in the hepatoprotection against LCA-induced intrahepatic cholestasis.
MedLine Citation:
PMID:  18032408     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The multidrug resistance-associated proteins (Mrps) are a family of adenosine triphosphate-dependent transporters that facilitate the movement of various compounds, including bile acids, out of hepatocytes. The current study was conducted to determine whether induction of these transporters alters bile acid disposition as a means of hepatoprotection during bile acid-induced cholestasis. Lithocholic acid (LCA) was used to induce intrahepatic cholestasis. C57BL/6 mice were pretreated with corn oil (CO) or known transporter inducers, phenobarbital (PB), oltipraz (OPZ), or TCPOBOP (TC) for 3 days prior to cotreatment with LCA and inducer for 4 days. Histopathology revealed that PB and TC pretreatments provide a protective effect from LCA-induced toxicity, whereas OPZ pretreatment did not. Both PB/LCA and TC/LCA cotreatment groups also had significantly lower alanine aminotransferase values than the LCA-only group. In TC/LCA cotreated mice compared with LCA only, messenger RNA (mRNA) expression of uptake transporters Ntcp and Oatp4 was significantly increased, as were sinusoidal efflux transporters Mrp3 and Mrp4. Although in PB/LCA cotreated mice, the only significant change compared with LCA-only treatment was an increase in uptake transporter Oatp4. Oatp1 was reduced in all groups compared with CO controls. No significant changes in mRNA expression were observed in Oatp2, Bsep, Mrp2, Bcrp, Mrp1, Mrp5, or Mrp6. Mrp4 protein expression was induced in the OPZ/LCA and TC/LCA cotreated groups, whereas Mrp3 protein levels remained unchanged between groups. Protein expression of Mrp1 and Mrp5 was increased in the unprotected LCA-only and OPZ/LCA mice. Thus, transporter expression did not correlate with histologic hepatoprotection, however, there was a correlation between hepatoprotection and significantly reduced total liver bile acids in the PB/LCA and TC/LCA cotreated mice compared with LCA only. In conclusion, changes in transporter expression did not correlate with hepatoprotection, and therefore, transport may not play a critical role in the observed hepatoprotection from LCA-induced cholestasis in the C57BL/6 mouse.
Authors:
Lisa D Beilke; David G Besselsen; Quiqiong Cheng; Supriya Kulkarni; Angela L Slitt; Nathan J Cherrington
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-11-20
Journal Detail:
Title:  Toxicological sciences : an official journal of the Society of Toxicology     Volume:  102     ISSN:  1096-6080     ISO Abbreviation:  Toxicol. Sci.     Publication Date:  2008 Mar 
Date Detail:
Created Date:  2008-02-07     Completed Date:  2008-04-10     Revised Date:  2013-05-23    
Medline Journal Info:
Nlm Unique ID:  9805461     Medline TA:  Toxicol Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  196-204     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Toxicology, College of Pharmacy, University Animal Care, University of Arizona, Tucson 85721, USA.
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MeSH Terms
Descriptor/Qualifier:
ATP-Binding Cassette Transporters / metabolism
Animals
Bile Acids and Salts / metabolism
Cholestasis, Intrahepatic / chemically induced,  genetics,  metabolism,  pathology,  prevention & control*
Cytoprotection
Disease Models, Animal
Lithocholic Acid
Liver / drug effects*,  enzymology,  metabolism,  pathology
Male
Membrane Transport Proteins / biosynthesis,  genetics,  metabolism*
Mice
Mice, Inbred C57BL
Multidrug Resistance-Associated Proteins / metabolism
Organic Anion Transporters / metabolism
Organic Anion Transporters, Sodium-Dependent / metabolism
Phenobarbital / pharmacology*,  therapeutic use
Protective Agents / pharmacology*,  therapeutic use
Pyrazines / pharmacology*,  therapeutic use
Pyridines / pharmacology*,  therapeutic use
RNA, Messenger / biosynthesis
Symporters / metabolism
Time Factors
Up-Regulation
Grant Support
ID/Acronym/Agency:
DK068039/DK/NIDDK NIH HHS; ES011646/ES/NIEHS NIH HHS; K22 ES011646/ES/NIEHS NIH HHS; K22 ES013782-01/ES/NIEHS NIH HHS; P20RR016457/RR/NCRR NIH HHS; R01 DK068039/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Bile Acids and Salts; 0/Membrane Transport Proteins; 0/Multidrug Resistance-Associated Proteins; 0/Organic Anion Transporters; 0/Organic Anion Transporters, Sodium-Dependent; 0/Protective Agents; 0/Pyrazines; 0/Pyridines; 0/RNA, Messenger; 0/Symporters; 145420-23-1/sodium-bile acid cotransporter; 434-13-9/Lithocholic Acid; 50-06-6/Phenobarbital; 6N510JUL1Y/oltipraz; 76150-91-9/1,4-bis(2-(3,5-dichloropyridyloxy))benzene

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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