Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Mitigation of TGF-^6;/Smad signaling pathway-associated liver fibrosis by paeoniflorin

Wen-Zhong Li, Zi-Bai Wei

Department of Gastroenterology, Heping Hospital Affiliated to Changzhi Medical College, No. 110 Yanâ€™an Road, Changzhi, Shanxi Province, 046000, China;

For correspondence:- Zi-Bai Wei Email: zibwei@163.com

Accepted: 24 August 2017 Published: 30 September 2017

Citation: Li W, Wei Z. Mitigation of TGF-^6;/Smad signaling pathway-associated liver fibrosis by paeoniflorin. Trop J Pharm Res 2017; 16(9):2107-2112 doi: 10.4314/tjpr.v16i9.9

© 2017 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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-^6;, Hepatic stellate cell, Smad, Hydroxyproline