Alpha-lipoic acid-induced heme oxygenase-1 expression is mediated by nuclear factor erythroid 2-related factor 2 and p38 mitogen-activated protein kinase in human monocytic cells

Arterioscler Thromb Vasc Biol. 2005 Oct;25(10):2100-5. doi: 10.1161/01.ATV.0000183745.37161.6e. Epub 2005 Aug 25.

Abstract

Objective: Heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, plays a protective role in the vascular system. HO-1 induction inhibits cytokine production in macrophages. Antioxidants induce HO-1 expression in various cell types. Alpha-lipoic acid (ALA), a thiol-containing dietary antioxidant, exhibits protective effects in vascular disease and induces anti-inflammatory effects in monocytes. This study examined the effects of ALA on HO-1 expression in human monocytic cells.

Methods and results: ALA time and dose-dependently induced HO-1 mRNA expression in THP-1 cells, with peak expression at 4 hours and returning to baseline by 24 hours. This correlated with an increase in HO-1 protein expression. ALA stimulated translocation of the transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf2) into the nucleus and binding to a human HO-1 antioxidant response element (ARE) by 30 minutes. A dominant-negative Nrf2 inhibitor reduced ALA-induced HO-1 mRNA expression by 66%. Pretreatment with SB203580, a p38 mitogen-activated protein kinase inhibitor, reduced ALA-induced HO-1 mRNA expression by 75% and inhibited ALA-induced Nrf2 binding to the HO-1 ARE.

Conclusions: These results demonstrate that ALA induces HO-1 expression in THP-1 monocytic cells via Nrf2 and p38. Further studies are required to investigate whether the protective effects of ALA in monocytes are mediated by HO-1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Active Transport, Cell Nucleus / drug effects
  • Cell Line, Tumor
  • Gene Expression / drug effects
  • Genes, Dominant
  • Heme Oxygenase-1 / genetics*
  • Heme Oxygenase-1 / metabolism
  • Humans
  • Leukemia
  • Monocytes / cytology
  • Monocytes / drug effects
  • Monocytes / physiology*
  • NF-E2-Related Factor 2 / genetics
  • NF-E2-Related Factor 2 / metabolism*
  • RNA, Messenger / analysis
  • Response Elements / physiology
  • Thioctic Acid / pharmacology*
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • RNA, Messenger
  • Thioctic Acid
  • Heme Oxygenase-1
  • p38 Mitogen-Activated Protein Kinases