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Antifibrotic compounds from Liriodendron tulipifera attenuating HSC-T6 proliferation and TNF-α production in RAW264.7

Eun Ju Jeong1, Na-Hyun Kim, Jeong-Doo Heo

  • 1Department of Agronomy & Medicinal Plant Resources, College of Life Sciences and Natural Resources, Gyeongnam National University of Science and Technology.

Biological & Pharmaceutical Bulletin
|March 10, 2015
PubMed

Insights

Liriodendron tulipifera extract inhibits liver fibrosis by reducing hepatic stellate cell proliferation. Key compounds like (-)-syringaresinol, (+)-dihydrodehydrodiconiferyl alcohol, and salvinal show potent antifibrotic effects without harming liver cells.

Area of Science:

  • Pharmacology
  • Natural Products Chemistry
  • Hepatology

Background:

  • Liver fibrosis is a significant health concern, with hepatic stellate cell (HSC) proliferation being a key therapeutic target.
  • Natural products offer potential avenues for developing novel antifibrotic agents.

Purpose of the Study:

  • To investigate the antifibrotic potential of Liriodendron tulipifera extract and identify active compounds.
  • To evaluate the efficacy and safety of isolated compounds in inhibiting HSC proliferation and related fibrotic processes.

Main Methods:

  • Bioactivity-guided isolation of compounds from L. tulipifera methanolic extract.
  • In vitro assays to assess inhibition of HSC proliferation (HSC-T6 cells).
  • Cytotoxicity testing on primary rat hepatocytes and assessment of collagen deposition and TNF-α production.

Main Results:

  • The L. tulipifera extract demonstrated significant inhibition of HSC proliferation.
  • Twelve compounds were isolated, with (-)-syringaresinol (2), (+)-dihydrodehydrodiconiferyl alcohol (3), and salvinal (4) showing potent antifibrotic activity.
  • Compounds 2, 3, and 4 reduced collagen deposition in HSCs and suppressed TNF-α production in macrophages without significant cytotoxicity to hepatocytes.

Conclusions:

  • (-)-Syringaresinol, (+)-dihydrodehydrodiconiferyl alcohol, and salvinal possess selective antifibrotic properties against activated HSCs.
  • These compounds also modulate pro-inflammatory responses, suggesting their potential as therapeutic candidates for liver fibrosis treatment.

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