Salvianolic acid B modulates the expression of drug-metabolizing enzymes in HepG2 cells

Hepatobiliary Pancreat Dis Int. 2011 Oct;10(5):502-8. doi: 10.1016/s1499-3872(11)60085-4.

Abstract

Background: Enzymes involved in drug and xenobiotic metabolism have been considered to exist in two groups: phase I and phase II enzymes. Cytochrome P450 isoenzymes (CYPs) are the most important phase I enzymes in the metabolism of xenobiotics. The products of phase I metabolism are then acted upon by phase II enzymes, including glutathione S-transferases (GSTs). Herbs that inhibit CYPs such as CYP3A4 or that induce GSTs may have the potential to protect against chemical carcinogenesis since the mutagenic effects of carcinogens are often mediated through an excess of CYP-generated reactive intermediates. This study was designed to investigate the effects of salvianolic acid B (Sal B), a pure compound extracted from Radix Salviae Miltiorrhizae, a Chinese herb, on cell proliferation and CYP1A2 and CYP3A4 mRNA expression in the presence or absence of rifampicin, a potent inducer of CYPs and GST protein expression in HepG2 cells.

Methods: HepG2 cells were incubated with different concentrations of Sal B. Cell proliferation was determined by SYTOX-Green nucleic acid staining. CYP3A4 and CYP1A2 mRNA expression was assayed by real-time PCR. GST protein expression was analyzed by Western blotting.

Results: Low concentrations of Sal B (0-20 μmol/L) had no significant effects on cell proliferation, while higher concentrations (100-250 μmol/L) significantly inhibited proliferation in a concentration-dependent manner. Ten μmol/L Sal B, but not 1 μmol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 μmol/L Sal B down-regulated CYP3A4 mRNA expression after 96 hours of incubation; moreover, 1 and 10 μmol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. Both 1 μmol/L and 10 μmol/L Sal B increased GST expression.

Conclusion: Sal B inhibits CYP3A4 and CYP1A2 mRNA expression and induces GST expression in HepG2 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Benzofurans / pharmacology*
  • Blotting, Western
  • Cell Proliferation / drug effects
  • Cytochrome P-450 CYP1A2 / biosynthesis
  • Cytochrome P-450 CYP1A2 / genetics*
  • Cytochrome P-450 CYP3A / biosynthesis
  • Cytochrome P-450 CYP3A / genetics*
  • Dose-Response Relationship, Drug
  • Enzyme Induction
  • Enzyme Repression
  • Gene Expression Regulation, Neoplastic / drug effects
  • Glutathione Transferase / biosynthesis
  • Hep G2 Cells
  • Humans
  • Liver Neoplasms / enzymology
  • Liver Neoplasms / genetics*
  • Liver Neoplasms / pathology
  • RNA, Messenger / metabolism
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Rifampin / pharmacology
  • Time Factors

Substances

  • Benzofurans
  • RNA, Messenger
  • salvianolic acid B
  • CYP1A2 protein, human
  • Cytochrome P-450 CYP1A2
  • Cytochrome P-450 CYP3A
  • CYP3A4 protein, human
  • Glutathione Transferase
  • Rifampin