Probucol inhibits lipid peroxidation of macrophage and affects its secretory properties

Acta Pharmacol Sin. 2000 Jul;21(7):637-40.

Abstract

Aim: To investigate the mechanisms of anti-atherogenic actions of probucol.

Methods: Human peripheral blood monocytes were cultured, and treated by copper ion (10 mumol/L) and/or probucol (PBC). Lipid peroxidation was measured by assaying malondialdehyde (MDA). The cytokine interleukin-1 beta (IL-1 beta) and apolipoprotein E (apo E) secreted by monocyte were assayed by enzyme linked immunoassay (ELISA).

Results: PBC 10-80 mumol/L inhibited copper ion-induced cellular lipid peroxidation from 15.30 to 7.74 mumol MDA/g cell protein. PBC 40 mumol/L inhibited oxidized macrophage-mediated oxidation of LDL from 5.18 to 1.65 mumol MDA/g cell protein, and attenuated secretory properties of monocytes induced by copper ion. The release of apo E, which is involved in reverse cholesterol transport, increased by 65%. And the release of IL-1 beta, which was shown to enhance vascular smooth muscle cell proliferation, decreased by 45%.

Conclusion: Probucol inhibits lipid peroxidation of macrophages and affects their secretory properties.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anticholesteremic Agents / pharmacology*
  • Apolipoproteins E / metabolism
  • Cells, Cultured
  • Humans
  • Interleukin-1 / metabolism
  • Lipid Peroxidation / drug effects*
  • Macrophages / metabolism*
  • Malondialdehyde / metabolism
  • Probucol / pharmacology*

Substances

  • Anticholesteremic Agents
  • Apolipoproteins E
  • Interleukin-1
  • Malondialdehyde
  • Probucol