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Published:
Oct 4, 2017DOI:
10.4314/tjpr.v16i9.9Keywords:
Article Details
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Main Article Content
Mitigation of TGF-β/Smad signaling pathway-associated liver fibrosis by paeoniflorin
Abstract
Purpose: To evaluate paeoniflorin (PF) as a possible protective agent against liver fibrosis and its likely mechanisms of action.
Methods: A rat model of liver fibrosis was induced by carbon tetrachloride (CCl4) injection. Liver damage was determined by serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. The hydroxyproline content of proteins was measured as an indirect way of assessing collagen deposition. TGF-β1 levels and TGF-β/Smad signaling pathway-related genes and proteins were analyzed by quantitative polymerase chain reaction (qPCR) assay and Western blot assay.
Results: After PF administration, serum ALT and AST levels were significantly (p < 0.01) reduced by 34.9 and 37.6 %, respectively. Collagen deposition was also significantly (p < 0.01) reduced by 31.0 %. Hepatic stellate cell activation was significantly inhibited, as evidenced by suppressed α-SMA expression. PF inhibited phospo-Smad 2/3 by elevating Smad 7 level.
Conclusion: PF alleviates CCl4-induced liver fibrosis in a dose-dependent manner probably by restoring the balance between activated Smad 2/3 and Smad7. Thus, PF might be a source of a novel anti-fibrotic agent.
Keywords: Paeoniflorin, Fibrosis, Liver, TGF-β, Hepatic stellate cell, Smad, Hydroxyproline
