Document Detail

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro-inflammatory factors in vivo and in vitro.
MedLine Citation:
PMID:  21265825     Owner:  NLM     Status:  MEDLINE    
BACKGROUND AND PURPOSE: Renal fibrosis acts as the common pathway leading to the development of end-stage renal disease. The present study investigated, in vivo and in vitro, the anti-fibrotic and anti-inflammatory effects, particularly on the epithelial to mesenchymal transition of renal tubular cells, exerted by honokiol, a phytochemical used in traditional medicine, and mechanisms underlying these effects.
EXPERIMENTAL APPROACH: Anti-fibrotic effects in vivo were assayed in a rat model of renal fibrosis [the unilateral ureteral obstruction (UUO) model]. A rat tubular epithelial cell line (NRK-52E) was stimulated by transforming growth factor-β1 (TGF-β1) and treated with honokiol to explore possible mechanisms of these anti-fibrotic effects. Gene or protein expression was analysed by Northern or Western blotting. Transcriptional regulation was investigated using luciferase activity driven by a connective tissue growth factor (CTGF) promoter.
KEY RESULTS: Honokiol slowed development of renal fibrosis both in vivo and in vitro. Honokiol treatment attenuated tubulointerstitial fibrosis and expression of pro-fibrotic factors in the UUO model. Honokiol also decreased expression of the mRNA for the chemokine CCL2 and for the intracellular adhesion molecule-1, as well as accumulation of type I (α1) collagen and fibronectin in UUO kidneys. Phosphorylation of Smad-2/3 induced by TGF-β1 and CTGF luciferase activity in renal tubular cells were also inhibited by honokiol.
CONCLUSIONS AND IMPLICATIONS: Honokiol suppressed expression of pro-fibrotic and pro-inflammatory factors and of extracellular matrix proteins. Honokiol may become a therapeutic agent to prevent renal fibrosis.
Chih-Kang Chiang; Meei-Ling Sheu; Yi-Wei Lin; Cheng-Tien Wu; Chin-Ching Yang; Min-Wei Chen; Kuan-Yu Hung; Kuan-Dun Wu; Shing-Hwa Liu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  British journal of pharmacology     Volume:  163     ISSN:  1476-5381     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-12     Completed Date:  2011-10-27     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  586-97     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
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MeSH Terms
Actins / metabolism
Biphenyl Compounds / pharmacology,  therapeutic use*
Cell Line
Chemokine CCL2 / genetics,  metabolism
Connective Tissue Growth Factor / genetics
Extracellular Matrix Proteins / metabolism
Genes, Reporter
Intercellular Adhesion Molecule-1 / genetics,  metabolism
Kidney / drug effects*,  pathology
Kidney Tubules / metabolism,  pathology
Lignans / pharmacology,  therapeutic use*
Luciferases / genetics,  metabolism
RNA, Messenger / metabolism
Rats, Wistar
Signal Transduction
Smad2 Protein / metabolism
Smad3 Protein / metabolism
Transforming Growth Factor beta1 / pharmacology
Ureteral Obstruction / drug therapy*,  pathology
Reg. No./Substance:
0/Actins; 0/Biphenyl Compounds; 0/Chemokine CCL2; 0/Extracellular Matrix Proteins; 0/Lignans; 0/RNA, Messenger; 0/Smad2 Protein; 0/Smad3 Protein; 0/Transforming Growth Factor beta1; 11513CCO0N/honokiol; 126547-89-5/Intercellular Adhesion Molecule-1; 139568-91-5/Connective Tissue Growth Factor; EC 1.13.12.-/Luciferases

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