Effects of neferine on TGF-β1 induced proliferation and gremlin expression in hepatic stellate cells

Authors

  • Xiaofei Li Department of Infectious Diseases, Yiwu Central Hospital, Zhejiang 322000
  • Lianqing Lou Department of Infectious Diseases, Yiwu Central Hospital, Zhejiang
  • Shuang Wu Department of Infectious Diseases, Yiwu Central Hospital, Zhejiang
  • Yongxin Chen Department of Infectious Diseases, Yiwu Central Hospital, Zhejiang
  • Lingzhen Jin Department of Infectious Diseases, Yiwu Central Hospital, Zhejiang

DOI:

https://doi.org/10.3329/bjp.v7i3.11298

Keywords:

Gremlin, Hepatic fibrosis, Neferine, Transforming growth factor-β1

Abstract

To clarify the possible molecular mechanism underlying the anti-fibrotic effect of neferine (Nef), we investigated the in vitro effects of Nef on the proliferation of hepatic stellate cells and expressions of gremlin, TGF-β1 and α-SMA in these cells. TGF-β1 had no influence on the proliferation of HSC-T6 cells (p>0.05) but significantly up-regulated the mRNA and protein expressions of gremlin, TGF-β1 and α- SMA in these cells (p<0.005). Nef could inhibit the proliferation of HSC-T6 cells in a dose and time dependent manner, and down-regulate the mRNA and protein expression of gremlin, TGF-β1 and α- SMA in these cells (p<0.005). Nef is an effective drug that can inhibit the proliferation of hepatic stellate cells to improve the hepatic fibrosis. Gremlin involves in the occurrence and development of hepatic fibrosis and may become a promising target in the treatment of hepatic fibrosis.

Downloads

Download data is not yet available.
Abstract
289
Download
92 Read
5

References

Boers W, Aarrass S, Linthorst C, Pinzani M, Elferink RO, Bosma P. Transcriptional profiling revealsnovel markers of liver fibrogenesis: gremlin and insulin - like growth factor - binding proteins. J Biol Chem. 2006; 281: 16289-95.

Costello CM, Cahill E, Martin F, Gaine S, McLoughlin P. Role of gremlin in the lung: Development and disease. Am J Respir Cell Mol Biol. 2010; 42: 517-23.

Ding H, Shi J, Wang Y, Guo J, Zhao J, Dong L. Neferine inhibits cultured hepatic stellate cell activation and facilitates apoptosis: A possible molecular mechanism. Eur J Pharmacol. 2011; 650: 163-69.

Huang C, Li Y, Cao P, Xie Z, Qin Z. Synergistic effect of hyperthermia and neferine on reverse multidrug resistance in adriamycin-resistant SGC7901/ADM gastric cancer cells. J Huazhong Univ Sci Technolog Med Sci. 2011; 31: 488-96.

Jung HA, Jin SE, Choi RJ, Kim DH, Kim YS, Ryu JH, Kim DW, Son YK, Park JJ, Choi JS. Anti-amnesic activity of neferine with antioxidant and anti-inflammatory capacities, as well as inhibition of ChEs and BACE1. Life Sci. 2010; 87: 420-30.

Sethi A, Jain A, Zode GS, Wordinger RJ, Clark AF. Role of TGFbeta/Smad signaling in gremlin induction of human trabecular meshwork extracellular matrix proteins. Invest Ophthalmol Vis Sci. 2011; 52: 5251-59.

Tacke F, Weiskirchen R. Liver fibrosis-pathogenesis and novel therapeutic approaches. Internist (Berl). 2010; 51: 21-29.

Xu L, Hui AY, Albanis E, Arthur MJ, O'Byrne SM, Blaner WS, Mukherjee P, Friedman SL, Eng FJ. Human hepatic stellate cell lines, LX-1 and LX-2: New tools for analysis of hepatic fibrosis. Gut 2005; 54: 142-51.

Zhang X, Liu Z, Xu B, Sun Z, Gong Y, Shao C. Neferine, an alkaloid ingredient in lotus seed embryo, inhibits proliferation of human osteosarcoma cells by promoting p38 MAPK-mediated p21 stabilization. Eur J Pharmacol. 2012; 677: 47-54.

Zhao L, Wang X, Chang Q, Xu J, Huang Y, Guo Q, Zhang S, Wang W, Chen X, Wang J. Neferine, a bisbenzylisoquinline alkaloid attenuates bleomycin-induced pulmonary fibrosis. Eur J Pharmacol. 2010; 627: 304-12.

Downloads

Additional Files

Published

2012-08-23

How to Cite

Li, X., L. Lou, S. Wu, Y. Chen, and L. Jin. “Effects of Neferine on TGF-β1 Induced Proliferation and Gremlin Expression in Hepatic Stellate Cells”. Bangladesh Journal of Pharmacology, vol. 7, no. 3, Aug. 2012, pp. 169-72, doi:10.3329/bjp.v7i3.11298.

Issue

Vol. 7 No. 3 (2012)

Section

Research Articles

License

Authors who publish with this journal agree to the following terms:

  1. Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
  2. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
  3. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).