These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Smad3 specific inhibitor, naringenin, decreases the expression of extracellular matrix induced by TGF-beta1 in cultured rat hepatic stellate cells.
    Author: Liu X, Wang W, Hu H, Tang N, Zhang C, Liang W, Wang M.
    Journal: Pharm Res; 2006 Jan; 23(1):82-9. PubMed ID: 16341574.
    Abstract:
    PURPOSE: During the process of liver fibrogenesis, transforming growth factor-beta (TGF-beta) plays an essential role in modulating extracellular matrix (ECM) gene expression, and a growing body of evidence suggests that this is a Smad3-dependent process in the activated hepatic stellate cells (HSCs). Naringenin showed a significantly protective effect on experimental rat liver fibrosis, in our efforts to elucidate its antifibrosis molecular mechanisms and to find a novel target based on Smad3 signaling for challenging fibrosis diseases. METHODS: In this study, reverse transcription-polymerase chain reaction and Western blot assays were used to investigate the inhibitory effect of naringenin on ECM formation induced by TGF-beta1 in the HSC-T6 cells. RESULTS: Naringenin reduced not only the accumulation of ECM, including collagen Ialpha1 (Col Ialpha1), fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1), but also the production of Smad3 induced by TGF-beta1 in both mRNA and protein levels in a dose-dependent manner. Moreover, naringenin selectively inhibited the transcription of Smad3, but not other Smads involved in TGF-beta1 signaling pathways. CONCLUSION: Our data demonstrate that naringenin can exert antifibrogenic effects by directly or indirectly down-regulating Smad3 protein expression and phosphorylation through TGF-beta signaling.
    [Abstract] [Full Text] [Related] [New Search]