Archives of Pharmacal Research

, 31:659

Effects of tanshinone IIA on the hepatotoxicity and gene expression involved in alcoholic liver disease

Authors

  • Hu-Quan Yin
    • College of Pharmacy and Research Institute of Pharmaceutical SciencesSeoul National University
  • Youn-Su Kim
    • College of Pharmacy and Research Institute of Pharmaceutical SciencesSeoul National University
  • You-Jin Choi
    • College of Pharmacy and Research Institute of Pharmaceutical SciencesSeoul National University
  • Youn-Chul Kim
    • College of PharmacyWonkwang University
    • College of Pharmacy and Research Institute of Pharmaceutical SciencesSeoul National University
  • Dong-Hwan Sohn
    • College of PharmacyWonkwang University
    • College of Pharmacy and Research Institute of Pharmaceutical SciencesSeoul National University
  • Shi-Yong Ryu
    • Korea Research Institute of Chemical Technology
    • College of Pharmacy and Research Institute of Pharmaceutical SciencesSeoul National University
    • College of Pharmacy and Research Institute of Pharmaceutical SciencesSeoul National University
Articles Drug Efficacy and Safety

DOI: 10.1007/s12272-001-1209-2

Cite this article as:
Yin, H., Kim, Y., Choi, Y. et al. Arch. Pharm. Res. (2008) 31: 659. doi:10.1007/s12272-001-1209-2

Abstract

Tanshinone IIA is one of the most abundant constituents of the root of Salvia miltiorrhiza BUNGE which exerts antioxidant and anti-inflammatory actions in many experimental disease models. In the present study, we demonstrated that the standardized fraction of S. miltiorrhiza (Sm-SF) was able to protect RAW 264.7 cells from ethanol-and lipopolysaccharide (LPS)-induced production of superoxide radical, activation of NADPH oxidase and subsequently death of the cells. Among four main components of Sm-SF, tanshinone IIA was the most potent in protecting cells from LPS-and ethanol-induced cytotoxicity. LPS or ethanol induced the expression of CD14, iNOS, and SCD1 and decreased RXR-α, which was completely reversed by tanshinone IIA. In H4IIEC3 cells, 10 μM tanshinone IIA effectively blocked ethanol-induced fat accumulation as evidenced by Nile Red binding assay. These results indicate that tanshinone IIA may have potential to inhibit alcoholic liver disease by reducing LPS-and ethanol-induced Kupffer cell sensitization, inhibiting synthesis of reactive oxygen/nitrogen species, inhibiting fatty acid synthesis and stimulating fatty acid oxidation.

Key words

Salvia miltiorrhizaTanshinone IIAAlcoholic liver diseaseOxidative stressLipid metabolism

Copyright information

© The Pharmaceutical Society of Korea 2008